Global7 the new Millennial Renaissance Vision for the Globe
Our Passion is 2 reach our individual & collective potential 4 excellence &Success-Always!
Global Patriotic Network Launches the COFFEE Party
(Coalition of Fair & Free Economic Enterprises!)
Promoting character, Leadership & integrity: protecting, preserving and promoting the Global Patriotic Future for the next generation!
The Global Patriotic Network is a public and private enterprise dedicated to protecting and preserving a Global Patriotic Future for the next generation across the globe
Our Passion
• To protect and preserve a Global Patriotic Future for the next generation
Our Value
• Character, leadership and integrity that promotes a sustainable secure future, based on good governance and aspiring for a progressive prosperity for all
Our Vision
• To galvanize all Global Citizens towards sustainable security, good governance and progressive prosperity for all
Our Mission
• To organize a series of win-win public private enterprises dedicated to nurture patriotism, character, leadership and integrity among all citizens of the globe
Our Strategic Goal
• To initiate a series of public and private networks of patriotism that promotes character, leadership and integrity at individual and collective social and economic life across all cultures
Our SMART Objectives
1. Specific: Promote character, leadership and integrity at individual and collective level across all communities regardless of age, gender, culture, color, race, nationality, religious and political affiliations
2. Measurable: Promote all activities against Qualitative and Quantitative tools the measure progress over time
3. Appropriate: Ensure that all activities are appropriate to the cultural diversity of communities at individual and collective level
4. Realistic: Develop realistic goals and targets that respect the resources and potential of each community at individual and collective level
5. Time Sensitive: Ensure that each activity is delivered in a specific time frame, within the talents and resources available to each partner communities
Global Patriotic Network will be headquartered in Washington, DC with global public and private networks both at the cyber and geographical domains without borders
Your creative and innovative response is appreciated.
Global Patriotic Network launches the first Global COFFEE (Coalition of Free & Fair Enterprises) Party designed to empower global citizens!
Global COFFEE Party is a public private enterprise designed to promote Global Coalition of Fair and Free Economic Enterprises across the globe to challenge the current global economic and ecological crisis.
The natural coffee plant is known to boost the immune system and our network of memories; the Global COFFEE Party is designed to simulate the Coffee plant that grows wild in the Kafa Province of Ethiopia to stimulate a global Coalition of Fair and Free Economic Enterprises
The Global COFFEE Party will support progressive scientific and evidence based ideas, policies, technologies that promote Fair, Free Economic Enterprises within the construct of Sustainable Security, Good Governance and Progressive Prosperity for all. Our passion to reach our individual and collective potential for excellence and success-Always.
The toxic financial and ecological assets are becoming a serious burden to the current and future generations. Well established institutions such as Harvard, Oxford and London Universities are known to produce the most toxic MBA and Economic graduates that have generated a series of voodoo economic policies, hedge funds and derivates that are not based on facts or science.
The Global COFFEE Party considers science, evidence based interactions supported by qualitative and quantitative research such as the Research Pyramid (that asks what, why, how, who, when and where questions); the CORT Analysis (that identifies, challenges, opportunities, risks and threats) towards converting all challenges into opportunities; as well as the NDSI Model (the Needs, Demands, Supply, Interaction Model:
Our Passion
• To protect and preserve and promote the a Global Patriotic Future for the next generation via win-win Global COFFEE Party that promotes economic enterprises!
Our Value
• Character, leadership and integrity that promotes a sustainable secure future, based on good governance and aspiring for a progressive prosperity for all
Our Vision
• To galvanize all Global Citizens towards sustainable security, good governance and progressive prosperity for all
Our Mission
• To organize a series of win-win public private enterprises dedicated to nurture patriotism, character, leadership and integrity among all citizens of the globe
Our Strategic Goal
• To initiate a series of public and private networks of patriotism that promotes character, leadership and integrity at individual and collective social and economic life across all cultures
Our SMART Objectives
6. Specific: Promote character, leadership and integrity at individual and collective level across all communities regardless of age, gender, culture, color, race, nationality, religious and political affiliations
7. Measurable: Promote all activities against Qualitative and Quantitative tools the measure progress over time
8. Appropriate: Ensure that all activities are appropriate to the cultural diversity of communities at individual and collective level
9. Realistic: Develop realistic goals and targets that respect the resources and potential of each community at individual and collective level
10. Time Sensitive: Ensure that each activity is delivered in a specific time frame, within the talents and resources available to each partner communities
Global Patriotic Network will be headquartered in Washington, DC with global public and private networks both at the cyber and geographical domains without borders
Your creative and innovative response is appreciated.
--
BFMHJ (BMJ)
Belai Habte-Jesus,MD,MPH
Global Strategic Enterprises,Inc
www.SolomonicCrown.org
Www.GlobalBelai4u.blogspot.com
V1=571.225.5736; V2= 703.933.8737; Fx1=202.3188277
GlobalBjesus@gmail.com;GloblBelaiJesus@me.com
Wednesday, November 24, 2010
Monday, November 22, 2010
Girma Wake of Ethiopian Airlines honored for saving Boeing and Ethiopian Airlines
Global7 the new Millennial Renaissance Vision for the Globe
CEO Girma Wake honored at Boeing 777 Delivery Dinner. Seattle, WA. Nov 20, 2010.
Boeing Co. honored the outgoing Ethiopian Airlines CEO Girma Wake at the 777-200LR delivery dinner held in Seattle, WA.
The dinner event was organized by Boeing Co. to celebrate the deliv- ery of its 900th 777 to the first and only African airlines.
Boeing recognized Mr. Wake for four decade of service in the avia- tion industry and for building and maintaining a mutually beneficial business relationship between Boeing and Ethiopian Airlines.
Boeing marketing vice president thanked Ethiopian Airlines for or- dering five 777 in 2009 when Boeing was considering closing produc- tion line due to the downturn in the world economy.
Ethiopian Airlines Board Chairman His Excellency Seyum Mesfin thanked Ato Girma for his dedicated service at Ethiopian Airlines. Ato Seyum said that while he discussed with over a hundred people for the Ethiopian CEO position almost all included Ato Girma in their recommendation as the person who could turn the declining air- lines around.
Ato Seyum appreciated Ato Girma for his sacrifice, dedication and commitment to serve his country.
Ato Girma left his lucrative employment with Gulf Air where he earned over eight thousand US Dollars a month to work at Ethiopia airlines earning less than five hundred dollars a month. The only benefit package he got was a company car.
Ato Girma successfully turned Ethiopia around. He is now leaving it behind as one of the most successful airlines in the world. He has also recruited a new generation of leaders that are ready to take the airlines to new heights.
Ato Girma described Boeing 777-200LR as a beautiful airplane capable of flying non-stop for 18 hours. The first of five delivery of 777-200LR is going to allow Ethiopian to fly non-stop from Addis Ababa to Washing- ton DC or to Beijing while carrying additional 100 passengers.
The event was attended by many Ethiopians living in Seattle. It was a delightful experience for attendees to hear Ethiopia mentioned in positive light.
Over 150 Ethiopians work at Boeing in different capacity and some of whom had participated in building the Ethiopian 777-200LR. At Girrma reminded Ethiopians to help build airplanes that are suitable to the unique Ethiopian conditions and to serve as a human bond between Ethiopia and United States.
CEO Girma Wake honored at Boeing 777 Delivery Dinner. Seattle, WA. Nov 20, 2010.
Boeing Co. honored the outgoing Ethiopian Airlines CEO Girma Wake at the 777-200LR delivery dinner held in Seattle, WA.
The dinner event was organized by Boeing Co. to celebrate the deliv- ery of its 900th 777 to the first and only African airlines.
Boeing recognized Mr. Wake for four decade of service in the avia- tion industry and for building and maintaining a mutually beneficial business relationship between Boeing and Ethiopian Airlines.
Boeing marketing vice president thanked Ethiopian Airlines for or- dering five 777 in 2009 when Boeing was considering closing produc- tion line due to the downturn in the world economy.
Ethiopian Airlines Board Chairman His Excellency Seyum Mesfin thanked Ato Girma for his dedicated service at Ethiopian Airlines. Ato Seyum said that while he discussed with over a hundred people for the Ethiopian CEO position almost all included Ato Girma in their recommendation as the person who could turn the declining air- lines around.
Ato Seyum appreciated Ato Girma for his sacrifice, dedication and commitment to serve his country.
Ato Girma left his lucrative employment with Gulf Air where he earned over eight thousand US Dollars a month to work at Ethiopia airlines earning less than five hundred dollars a month. The only benefit package he got was a company car.
Ato Girma successfully turned Ethiopia around. He is now leaving it behind as one of the most successful airlines in the world. He has also recruited a new generation of leaders that are ready to take the airlines to new heights.
Ato Girma described Boeing 777-200LR as a beautiful airplane capable of flying non-stop for 18 hours. The first of five delivery of 777-200LR is going to allow Ethiopian to fly non-stop from Addis Ababa to Washing- ton DC or to Beijing while carrying additional 100 passengers.
The event was attended by many Ethiopians living in Seattle. It was a delightful experience for attendees to hear Ethiopia mentioned in positive light.
Over 150 Ethiopians work at Boeing in different capacity and some of whom had participated in building the Ethiopian 777-200LR. At Girrma reminded Ethiopians to help build airplanes that are suitable to the unique Ethiopian conditions and to serve as a human bond between Ethiopia and United States.
Wednesday, October 13, 2010
HIV Pandenic the new genocide among African Americans
Global7 the new Millennial Renaissance Vision for the Globe
The edge boston.com
HIV/AIDS Rate in America’s Capitol Exceeds Some African Nations
by Kilian Melloy
EDGE Contributor
Monday Mar 16, 2009
Dr. Anthony Fauci, NIH infectious diseases program director
A new report shows that the HIV/AIDS epidemic in Washington, D.C., are "higher than West Africa" HIV rates, and that heterosexual transmission of the disease is increasing, although the highest incidence new infections is still among men who have sex with men.
The Washington Post reported on the new study, which only accounts for Washington, D.C. residents who have gotten tested, prompting the report’s authors to note, "we know that the true number of residents currently infected and living with HIV is certainly higher."
A one percent rate of infection would be enough to regard the epidemic as "generalized and severe," the article noted.
The article quoted Washington, D.C. HIV/AIDS Administration director Shannon L. Hader, who said, "Our rates are higher than West Africa."
Added Hader, "They’re on par with Uganda and some parts of Kenya."
Hader noted, "We have every mode of transmission going up, all on the rise, and we have to deal with them."
The principle modes of HIV transmission are unprotected sex between men, unprotected heterosexual sex, and intravenous drug use, the article said. The new report shows a 22% increase in HIV/AIDS over three years ago.
The increase is discernible in all demographics, whether racial or geographical. African-American men were hardest hit, the study indicated: the demographic alone showed a seven percent infection rate, with 33% of African American men who were HIV positive reportedly contracting the virus through heterosexual contact.
Three percent African American women in the District are HIV positive, the report says, due to increasing transmission through heterosexual contact.
Among Caucasians, over three-quarters of HIV cases (78%) were among men who have sex with men; among Latinos, sexual contact among men accounted for 49% of infections, the article said.
Only one ward out of the District’s eight wards did not reflect an increase in HIV/AIDS rates, a development that the report anticipated would "have significant implications on the District’s health care system," the article reported.
A separate report prepared by George Washington University’s School of Health and Health Services looks more closely at heterosexual transmission of HIV, noting that only three out of ten heterosexual respondents reported using condoms during their most recent sexual encounters, while three out of five said that they knew whether they were HIV positive or negative.
The National Institutes of Health’s infectious diseases program director was quoted in the article.
Said Dr. Anthony Fauci, "This is very, very depressing news, especially considering HIV’s profound impact on minority communities."
Added Fauci, "And remember, the city’s numbers are just based on people who’ve gotten tested."
Said D.C. resident Ron Simmons, a gay African American, "You have a high incidence of HIV among African Americans, and a lot of African Americans live in the city."
Simmons, who the article said is with a support group, went on to say, "D.C. also has a high number of gay men, and HIV is high among gay black men."
Said Charlene Cotton, a D.C. resident who was diagnosed as positive five years ago, "You need to start at home and talk about it."
Added Cotton, "It’s so hush-hush."
Said Washington, D.C. mayor Adrian Fenty, "In order to solve an issue as complex as HIV and AIDS, you have to step up," the article said.
"It’s the mayor and certainly other elected officials. But it’s also the community.
"You have this problem affecting us, and you tell people how serious it is and it literally goes in one ear and out the other."
But D.C. city councilor David Catina, who chairs the city council’s health committee, had hard words for the District’s government, saying, "Frankly, there can be no excuse for the state of the HIV/AIDS Administration that I found in 2005.
"I cannot speak to why it was not a priority previously" added Catina. "For years prior to 2005, mayors and previous individuals allowed things to exist in an unacceptable way.
"And I do blame this government for part of the epidemic we’re confronting," Catina added.
The article said that the AIDS Office had lacked resources, and that the office’s critics had voiced doubts about the way its existing resources had been used.
Also called into question was a Congressional ban on using District tax revenue for needle exchange programs, possibly driving the infection rate higher. The article noted that the ban had been rescinded in 2008.
The one bright spot in the report was an indication that more people are getting tested, leading to earlier detection for those who are HIV positive. Early detection and medication is crucial in ensuring that HIV positive individuals live longer lives and enjoy better health.
The article tied the improvement in early detection to the fact that publicly funded testing had enjoyed a 70% increase over the last three years.
Kilian Melloy reviews media, conducts interviews, and writes commentary for EDGEBoston, where he also serves as Assistant Arts Editor.
The edge boston.com
HIV/AIDS Rate in America’s Capitol Exceeds Some African Nations
by Kilian Melloy
EDGE Contributor
Monday Mar 16, 2009
Dr. Anthony Fauci, NIH infectious diseases program director
A new report shows that the HIV/AIDS epidemic in Washington, D.C., are "higher than West Africa" HIV rates, and that heterosexual transmission of the disease is increasing, although the highest incidence new infections is still among men who have sex with men.
The Washington Post reported on the new study, which only accounts for Washington, D.C. residents who have gotten tested, prompting the report’s authors to note, "we know that the true number of residents currently infected and living with HIV is certainly higher."
A one percent rate of infection would be enough to regard the epidemic as "generalized and severe," the article noted.
The article quoted Washington, D.C. HIV/AIDS Administration director Shannon L. Hader, who said, "Our rates are higher than West Africa."
Added Hader, "They’re on par with Uganda and some parts of Kenya."
Hader noted, "We have every mode of transmission going up, all on the rise, and we have to deal with them."
The principle modes of HIV transmission are unprotected sex between men, unprotected heterosexual sex, and intravenous drug use, the article said. The new report shows a 22% increase in HIV/AIDS over three years ago.
The increase is discernible in all demographics, whether racial or geographical. African-American men were hardest hit, the study indicated: the demographic alone showed a seven percent infection rate, with 33% of African American men who were HIV positive reportedly contracting the virus through heterosexual contact.
Three percent African American women in the District are HIV positive, the report says, due to increasing transmission through heterosexual contact.
Among Caucasians, over three-quarters of HIV cases (78%) were among men who have sex with men; among Latinos, sexual contact among men accounted for 49% of infections, the article said.
Only one ward out of the District’s eight wards did not reflect an increase in HIV/AIDS rates, a development that the report anticipated would "have significant implications on the District’s health care system," the article reported.
A separate report prepared by George Washington University’s School of Health and Health Services looks more closely at heterosexual transmission of HIV, noting that only three out of ten heterosexual respondents reported using condoms during their most recent sexual encounters, while three out of five said that they knew whether they were HIV positive or negative.
The National Institutes of Health’s infectious diseases program director was quoted in the article.
Said Dr. Anthony Fauci, "This is very, very depressing news, especially considering HIV’s profound impact on minority communities."
Added Fauci, "And remember, the city’s numbers are just based on people who’ve gotten tested."
Said D.C. resident Ron Simmons, a gay African American, "You have a high incidence of HIV among African Americans, and a lot of African Americans live in the city."
Simmons, who the article said is with a support group, went on to say, "D.C. also has a high number of gay men, and HIV is high among gay black men."
Said Charlene Cotton, a D.C. resident who was diagnosed as positive five years ago, "You need to start at home and talk about it."
Added Cotton, "It’s so hush-hush."
Said Washington, D.C. mayor Adrian Fenty, "In order to solve an issue as complex as HIV and AIDS, you have to step up," the article said.
"It’s the mayor and certainly other elected officials. But it’s also the community.
"You have this problem affecting us, and you tell people how serious it is and it literally goes in one ear and out the other."
But D.C. city councilor David Catina, who chairs the city council’s health committee, had hard words for the District’s government, saying, "Frankly, there can be no excuse for the state of the HIV/AIDS Administration that I found in 2005.
"I cannot speak to why it was not a priority previously" added Catina. "For years prior to 2005, mayors and previous individuals allowed things to exist in an unacceptable way.
"And I do blame this government for part of the epidemic we’re confronting," Catina added.
The article said that the AIDS Office had lacked resources, and that the office’s critics had voiced doubts about the way its existing resources had been used.
Also called into question was a Congressional ban on using District tax revenue for needle exchange programs, possibly driving the infection rate higher. The article noted that the ban had been rescinded in 2008.
The one bright spot in the report was an indication that more people are getting tested, leading to earlier detection for those who are HIV positive. Early detection and medication is crucial in ensuring that HIV positive individuals live longer lives and enjoy better health.
The article tied the improvement in early detection to the fact that publicly funded testing had enjoyed a 70% increase over the last three years.
Kilian Melloy reviews media, conducts interviews, and writes commentary for EDGEBoston, where he also serves as Assistant Arts Editor.
Alternative perspective on Vaccine Science? or another Witchcraft?
Global7 the new Millennial Renaissance Vision for the Globe,
Our Passion is to reach our individual and collective potential-Always!
Millennium Wellness Enterprises, inc
Wellness can be a profitable enterprise as well people and fit people can continue to be productive, creative and enterprising. Sick people tend to be disabled and lose their productivity over time.
So, it is sound business practice and social practice to stay healthy, well and fit.
Unfortunately, we do not spend time on getting fit, healthy and well as these attributes are not converted into risk management insurance premiums and have value attached to them.
As a result, the medical industry is creating disease via vaccines, to imitate disease and sell the product as beneficial to the unsuspecting public via highly exaggerated scientific credo that has not been yet proven of its benefits.
The scientific tools and models of Risk assessment demand, the pragmatic use of Scientific tools such as Research Pyramid, CORT Analysis, NDSIM, 3As and 3Es and FoC as well as Option Appraisals.
Risk management strategy demands that we under take, Research Pyramid questions of what, why, how, who, when and where to understand the cause and effect relationships. CORT Analysis demands that we look at challenges, opportunities, risks and threats in detail and convert our challenges into opportunities. Most importantly the NDSIM, the Needs, Demands, Supply Interaction Model demands that we look at the question of 3As and 3Es, that is Accessibility, Afford ability, Accountability, in line with Equity, Efficiency and Effectiveness and their delivery in an environment of Freedom of Choice.
Option Appraisal science demands that we look at options and alternatives as well as making choices in the principle of Best Option, Win-Win Option and Compromise Option for an improved opportunity of success.
So, where does vaccine science fall within this bigger picture of empirical science for wellness and optimum health.
It is important to consider wellness science as an alternative to health science, as traditional perspectives have converted health science into sickness science.
The Medical profession is about producing medicines, marketing them and selling them to the public to make profit. However, this does not sound enlightened, so disease and sickness will be through in the mix to make it sound scientific and beneficial to humanity. After all, we are
talking about recovery or the healing profession.
The real science is about staying healthy and well. So, wellness demands pre-emptive fitness and optimum wellness strategy.
All the same it is critical that we appreciate that vaccines should be made accountable to our value system of optimum health and sustainable wellness.
Dr Belai Habte-Jesus
Millennium Wellness Enterprises, Inc
Evidence-based vaccinations: A scientific look at the missing science behind flu season vaccines
Thursday, September 02, 2010
by Mike Adams, the Health Ranger
Editor of NaturalNews.com (See all articles...)
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(NaturalNews) As someone with a good deal of education in scientific thinking and the scientific method, I have put considerable effort into attempting to find any real scientific evidence backing the widespread use of influenza vaccines (flu season shots). Before learning about nutrition and holistic health, I was a computer software entrepreneur, and I have a considerable scientific background in areas such as astronomy, physics, human physiology, microbiology, genetics, anthropology and human psychology. One of my most-admired thought leaders is, in fact, the late physicist Richard Feynman.
I don't speak from a "scientific" point of view on NaturalNews very often because it's often a dry, boring presentation style. But I do know the difference between real science and junk science, and I find examples of junk science in both the "scientific" side of things as well as the "alternative" side of things.
For example, so-called "psychic surgery," as least in the way it has been popularized, is nothing more than clever sleight-of-hand where the surgeon palms some chicken gizzards and then pretends to pull diseased organs out of the abdominal cavity of some patient. The demonstrations I've seen on film are obvious quackery.
Similarly, flu season vaccines are mainstream medicine's version of psychic surgery: It's all just "medical sleight of hand" based on nothing more than clever distractions and the obfuscation of scientific facts. Flu season shots, you see, simply don't work on 99 out of 100 people (and that's being generous to the vaccine industry, as you'll see below).
A year ago, I offered a $10,000 reward to any person who could find scientific proof that H1N1 vaccines were safe and effective (http://www.naturalnews.com/027985_H...). No one even made a claim to collect that reward because no such evidence exists.
Conventional medicine, they say, is really "Evidence-Based Medicine" (EBM). That is, everything promoted by conventional medicine is supposed to be based on "rigorous scientific scrutiny." It's all supposed to be statistically validated and proven beyond a shadow of a doubt that it works as advertised. And in the case of flu vaccines, they are advertised as providing some sort of absolute protection against influenza. "Don't miss work this flu season. Get a flu shot!" The idea, of course, is that getting a flu shot offers 100% protection from the flu. If you get a shot, they say, you won't miss work from sickness.
This implication is wildly inaccurate. In fact, it's just flat-out false. As you'll see below, it's false advertising wrapped around junk science.
You see, there was never an independent, randomized, double-blind, placebo-controlled study proving either the safety or effectiveness of the H1N1 swine flu vaccines that were heavily pushed last year (and are in fact in this year's flu shot cocktail). No such study has ever been done. As a result, there is no rigorous scientific basis from which to sell such vaccines in the first place.
To try to excuse this, vaccine hucksters claim that it would be "unethical" to conduct a placebo-controlled study of such vaccines because they work so well that to deny the placebo group the actual vaccine would be harmful to them. Everybody benefits from the influenza vaccine, they insist, so the mere act of conducting a scientifically-controlled test is unethical.
Do you smell some quackery at work yet? This is precisely the kind of pseudoscientific gobbledygook you might hear from some mad Russian scientist who claims to have "magic water" but you can't test the magic water because the mere presence of measurement instruments nullifies the magical properties of the water.
Similarly, vaccine pushers often insist it's unethical to test whether their vaccines really work. You just have to "take it on faith" that vaccines are universally good for everybody.
Yep, I used the word "faith." That is essentially what the so-called scientific community is invoking here with the vaccine issue: Just BELIEVE they work, everybody! Who needs scientific evidence when we've got FAITH in vaccines?
Forget about evidence-based medicine. Forget about any rational cost-benefit analysis. Forget about the risk-to-benefit ratio calculations that should be part of any rational decision making about vaccines. No, the vaccine industry (and its apologist bloggers) already know that vaccines are universally good for you, therefore no such rigorous scientific assessment is even required!
The Scientific Method, in other words, doesn't really apply to the things they already believe in. Faith can override reason in the "scientific" community, if you can believe that! What's next, are they going to claim vaccines work because some sort of "vaccine God" makes them work?
Here, take your vaccine shot. And don't forget to pray to the Vaccine God because that's how these things really work. Vaccine voodoo, in other words. (Hey, that would have been a great title for the vaccine song, come to think of it...)
Unethical to find out if they work?
I got to wondering about the whole explanation of how it would be "unethical" to test whether the H1N1 vaccines actually work. This deflection strikes me as particularly odd, because it comes with an implied follow-up statement. Here's what they're actually saying when they invoke this excuse:
#1) It is "unethical" to conduct placebo-controlled studies on seasonal flu vaccines to find out if they actually work.
#2) But at the same time, it is entirely ethical to give these shots to hundreds of millions of people, even while lacking any real evidence that they are safe or effective.
In other words, it's unethical to conduct any real science, but entirely ethical to just keep injecting people with a substance that might be entirely useless (or even harmful). That's just a hint of the kind of warped logic and failed ethics that typify our modern vaccine industry.
Vaccine advocates claim that H1N1 vaccines are so effective that NOT giving vaccines to a placebo group would "put their lives at risk." That alone is apparently enough reason to avoid conducting any real science on these vaccines.
But I'm not buying this. I think it's just a cover story -- an excuse to avoid subjecting such vaccines to rigorous scientific inquiry because, deep down inside, they know vaccines would be revealed as an elaborate medical fraud.
So I poked around to see if there were other randomized studies being conducted that might actually put people's lives at risk. It didn't take long to find some. For example, the New England Journal of Medicine recently published two studies regarding post heart-attack patient cooling which seeks to minimize brain damage by physically lowering the temperature of the brain of the heart attack patient until they can reach the acute care technicians at a nearby hospital.
In two studies, researchers who already knew that "cooling" would save lives nevertheless subjected 350 heart attack patient to a randomized study protocol that assigned comatose (but resuscitated) patients to either "cooling" temperatures or normal temperatures.
In one study, while half the cooled patients recovered with normal brain function, only a quarter of those exposed to normal temperatures did. In other words, patient cooling saved their brains. And yet the importance of knowing whether or not this procedure really worked was apparently enough to justify withholding the treatment from over a hundred other patients, most of whom suffered permanent brain damage as a result.
You see, when scientists really want to know the answers to questions like, "Does this brain cooling work?" they have no qualms about subjecting people to things like permanent brain damage in a randomized clinical trial. The knowledge gained from such an experiment is arguably worth the loss of a few patient brains because, armed with scientific evidence, such procedures can be rolled out to help save the brains of potentially hundreds of thousands of patients in subsequent years.
But when it comes to testing vaccines like the recent H1N1 variety, the official explanation is that it's too dangerous to withhold vaccines from a treatment group. They say it's not really important to determine if vaccines are statistically validated, and it's not worth the "risk" of withholding vaccines from anyone in a randomized clinical trial.
Now, sure, there have been some clinical trials done on many different vaccines over the years, but most of those are industry funded, and there are almost never rigorous trials conducted on each year's seasonal flu vaccines before they are released for public consumption. As a result, each year's vaccine is a brand new experiment, carried out across the guinea pig masses of patients who just do whatever they're told without questioning whether it's backed by real science.
Because, of course, it isn't. And I'm not the only one who recognizes this inconvenient fact.
The Cochrane Collaboration
The Cochrane Collaboration, as described on its own website, is, "...an international, independent, not-for-profit organization of over 28,000 contributors from more than 100 countries, dedicated to making up-to-date, accurate information about the effects of health care readily available worldwide."
"We are world leaders in evidence-based health care," the site goes on to say, followed by a quote from The Lancet which states, "The Cochrane Collaboration is an enterprise that rivals the Human Genome Project in its potential implications for modern medicine."
Working for the Cochrane Collaboration, an epidemiologist named Dr. Tom Jefferson decided to take a close look at the scientific evidence behind influenza vaccines (seasonal flu vaccines).
The objectives of the study were to: "Identify, retrieve and assess all studies evaluating the effects of vaccines against influenza in healthy adults."
The Search Criteria: "We searched the Cochrane Central Register of Controlled Trials (CENTRAL) (The Cochrane Library, 2010, issue 2), MEDLINE (January 1966 to June 2010) and EMBASE (1990 to June 2010)."
Selection Criteria (for inclusion in the study): "Randomized controlled trials (RCTs) or quasi-RCTs comparing influenza vaccines with placebo or no intervention in naturally-occurring influenza in healthy individuals aged 16 to 65 years. We also included comparative studies assessing serious and rare harms."
The Total Scope of the study encompassed over 70,000 people. And just so you know, these the results may strongly favor the vaccine industry. The author even went out of his way to warn that "15 out of 36 trials [were] funded by industry (four had no funding declaration)."
In other words, close to half of the studies included in this analysis were funded by the vaccine industry itself, which as we know consistently manipulates data, bribes researchers or otherwise engages in scientific fraud in order to get the results they want.
The author even goes on to warn how industry-funded studies always get more press, saying, "...industry funded studies were published in more prestigious journals and cited more than other studies independently from methodological quality and size."
See the study detail page at: http://onlinelibrary.wiley.com/o/co...
Study results show influenza vaccines are nearly worthless
Now here comes the interesting part: Even though nearly half the studies were funded by the vaccine industry itself, the study results show that in most circumstances, influenza vaccines are virtually worthless:
"The corresponding figures [of people showing influenza symptoms] for poor vaccine matching were 2% and 1% (RD 1, 95% CI 0% to 3%)" say the study authors. And by "poor vaccine matching," they mean that the strain of influenza viruses in the vaccine are a poor match for the strains circulating in the wild. This is usually the case in the real world because the vaccine only incorporates last year's viral strains and cannot predict which strains will be circulating this year.
In other words, you would have to vaccinate 100 people to reduce the number of people showing influenza symptoms by just one. For ninety-nine percent of the people vaccinated, the vaccine makes no difference at all!
In a "best case" scenario when the viral strain in the influenza vaccine just happens to match the strain circulating in the wild -- a situation that even the study authors call "uncommon" -- the results were as follows: "4% of unvaccinated people versus 1% of vaccinated people developed influenza symptoms (risk difference (RD) 3%, 95% confidence interval (CI) 2% to 5%)."
In other words, the matching vaccine (which is uncommon in the real world) reduced influenza infections in 3 out of 100 people. Or, put another way, 97% of those injected with the vaccine received no benefit (and no different outcome).
Furthermore, the study's conclusions go on to state:
• "Vaccination had... no effect on hospital admissions or complication rates."
• "Vaccine use did not affect the number of people hospitalized or working days lost."
• "The review showed that reliable evidence on influenza vaccines is thin but there is evidence of widespread manipulation of conclusions..."
• "There is no evidence that [influenza vaccines] affect complications, such as pneumonia, or transmission." (Got that? Vaccines do not affect transmission of the disease, yet that's the whole reason vaccines are pushed so heavily during pandemics -- to block disease transmission.)
• "In average conditions (partially matching vaccine) 100 people need to be vaccinated to avoid one set of influenza symptoms."
And finally, the study author's summary concludes with this whopper of a statement: "Our results may be an optimistic estimate because company-sponsored influenza vaccines trials tend to produce results favorable to their products and some of the evidence comes from trials carried out in ideal viral circulation and matching conditions and because the harms evidence base is limited."
In other words, taking into account the industry bias, the actual results may be that vaccines prevent influenza symptoms in only 1 out of 1,000 people.
Putting it in perspective
So let's put all this in perspective in a rational, intelligent way. This far-reaching analysis of influenza vaccine trials shows that under common conditions, seasonal influenza vaccines have no benefit for 99 out of 100 people.
Furthermore, even this result is describe as being "an optimistic estimate" because nearly half of the vaccine trials were funded by the vaccine industry which tends to "produce results favorable to their products."
Furthermore, some of the studies were carried out in "ideal" viral matching scenarios that rarely happen in the real world.
And finally, some evidence of harm from vaccines was simply thrown out of this analysis, resulting in a "harms evidence base" that was quite limited and likely doesn't reveal the full picture.
Are you getting all this? Even with industry-funded studies likely distorting the results in their favor, if you take a good hard look at the scientific evidence surrounding the effectiveness of vaccines, you quickly come to realize that influenza vaccines don't work on 99 out of 100 people. (And the real answer may be even worse.)
Now that's a far cry from the false advertising of the vaccine industry, which implies that if you get a shot you're "protected" from influenza. They claim you won't miss work, you'll stay well, and so on. Through these messages, they are cleverly implying that vaccines work on 100% of the people.
But based on the available scientific evidence, these are blatantly false statements. And the wild exaggeration of the supposed benefits from vaccines crosses the threshold of "misleading advertising" and enters the realm of "criminal marketing fraud." Where is the FTC or FDA on speaking out against this quackery?
Vaccine marketing is, essentially, scientific fraud. To claim that vaccines protect everyone when, in reality, they may reduce symptoms in only one out of 100 people is intellectually dishonest and downright fraudulent.
It is, simply put, just pure B.S. quackery.
Now, imagine if an herbal product were advertised on television as offering some health benefit, but it turned out that the product only worked on 1 out of 100 people who took it. That herbal product would be widely branded as "quackery" and the company selling it would be accused of false advertising. The company owners might even be charged with criminal fraud.
But vaccines get a free pass on this issue. While an herbal product might be heavily investigated or even confiscated by the FDA, vaccines that only work on 1% of the people receive the full backing of the FDA, CDC, WHO, FTC and local hospitals and clinics to boot. The fact that the vaccine is pure quackery apparently doesn't matter to any of these organizations: It's full speed ahead, regardless of what the science actually says.
Once you understand all this, you now understand why it is an accurate statement to say "The FDA promotes medical fraud."
Similarly, "The CDC promotes medical fraud." As does the WHO.
These are scientifically accurate statements, assuming you agree that a product that only works on 1 out of 100 people fits the definition of "fraud" when it is marketed as if it helped everyone. And most people would agree with that reasonable definition of fraud.
It's a totally different story if the efficacy ratio is higher. If influenza vaccines actually produced some benefit in 25 out of 100 people, that might be worth considering. But it's nowhere near that.
The FDA, by the way, will often approve pharmaceuticals that only produce results in 5 percent of the clinical trial subjects. The world of modern medicine, in fact, is full of pharmaceuticals that simply don't work on 95% of the patients who take them.
Read the Cochrane summary yourself at:
http://onlinelibrary.wiley.com/o/co...
It's entitled, "Vaccines for preventing influenza in healthy adults"
Authors: "Tom Jefferson, Carlo Di Pietrantonj, Alessandro Rivetti, Ghada A Bawazeer, Lubna A Al-Ansary, Eliana Ferroni"
Enter the vaccine zombies!
With these study results in mind, take a look at some of the lyrics in my recent hip hop song, "Vaccine Zombie" (http://www.naturalnews.com/vaccine_...)
I forgot how to think for myself
I don't understand a thing about health
I do the same as everyone else
I'm a vaccine zombie, zombie
Now you can see where these lyrics come from. If influenza vaccines are worthless for 99 percent of those who receive them, then why are people lining up to get injected?
The answer is because they fail to think critically about vaccines and their health. They don't understand health, so they just go along with everybody else and do what they're told. Hence their earning of the "Vaccine Zombie" designation.
The song goes on to say:
I'm a sucker for the ads, a sucker for the labs
A sucker for the swine flu jabs
and I don't mind followin' a medical fad
Cause livin' without a brain ain't half bad
Yes, people who line up for influenza vaccines are "suckers" who have been bamboozled by fraudulent vaccine propaganda. But they're following a "medical fad" and it's easier to just do what you're told rather than engage your brain and think critically about what you're doing.
"Livin' without a brain ain't half bad" because it takes the burden of decision making out of the loop and allows you to just rely on whatever the doctors and health officials tell you to do.
How the scientific community lost touch with real science
But what if they were all lying to you? Or what if they, themselves, were ignorant about the fact that influenza vaccines are worthless on 99% of those who receive them? (Very few doctors and scientists, it turns out, are aware of this simple truth.)
Or what if the vaccine pushers had all convinced themselves of a falsehood? What if they truly believed that vaccines were really, really good for everyone but that belief was based on wishful thinking rather than rigorous scientific review?
Because that, my friends, is exactly what has happened. We have an entire segment of the scientific community that has been suckered into vaccine propaganda. They've convinced themselves that seasonal flu shots really work and that virtually everyone should be injected with such shots. And they believe this based on irrational faith, not on scientific thinking or rigorous statistical evidence.
They are, in other words, pursuing a vaccine religion (or cult). The is especially curious, given that most vaccine pushers don't believe in God or any organized religion -- except for their own vaccine religion, where real scientific evidence isn't required. All you gotta do is believe in vaccines and you can join their religion, too.
And so all across the 'net, so-called "science bloggers" embarrass themselves by promoting near-useless influenza vaccines as "evidence-based medicine," apparently unaware that the evidence shows such vaccines to be all but worthless.
They might as well say they support vaccines "Just 'cuz."
And "just 'cuz" is no reason to inject yourself with a chemical cocktail that even the industry admits causes extremely dangerous neurological side effects in a small number of vaccine recipients.
Vitamin D would actually make vaccines work better
To top this all off, here's the real kicker of this story: You can beat the minimal protective benefits of vaccines with a simple, low-cost vitamin D supplement. Vitamin D, you see, is the nutrient that activates your immune system to fight off infectious disease. Without it, vaccines hardly work at all.
In fact, the very low rate of vaccine efficacy (1%) is almost certainly due to the fact that most people receiving the vaccines are vitamin D deficient. (Anywhere from 75% - 95% of Americans are deficient in vitamin D, depending on whom you ask.)
Hilariously, the way to make vaccines work better would be to hand out vitamin D supplements to go along with the shots! Even more hilariously, if people were taking vitamin D supplements, they wouldn't need the vaccine shots in the first place!
Influenza vaccines, in other words, have no important role whatsoever in preventing influenza infections. This goal can be accomplished more safely, reliably and at far lower cost by promoting vitamin D supplements for the population at large.
What we really need to see from the scientific world is a study comparing vitamin D supplements to influenza vaccines (and using realistic vitamin D doses, not just 200 or 400 IUs per day). I have absolutely no doubt that healthy-dose vitamin D supplementation (4000 IUs a day) would prove to be significantly more effective than influenza vaccines at preventing flu infections.
But such a study will almost certainly never be done (at least not anytime soon) because it would expose the false propaganda of the vaccine industry while giving consumers a far better way of protecting themselves from influenza that doesn't involve paying money to vaccine manufacturers.
In medicine, as in war, truth is often the first casualty. And when the lies are repeated with enough frequency, they begin to be believed. The flu shot lie has been repeated with such ferocity and apparent authority that it has snookered in virtually the entire "scientific" community.
That even rational-minded scientists can be so easily hoodwinked by the vaccine industry is causing more and more people to question the credibility of not just modern medicine, but the entire scientific community as well.
Because if so-called "rational" scientists and thought leaders can be so easily suckered into an obvious falsehood, what other fictions might they be promoting as fact?
Medicine, you see, makes all the other sciences look bad. The obvious scientific fraud going on in the name of "science" in the pharmaceutical industry makes a mockery of real scientific thought. The ease of which medical scientists have been hoodwinked by the drug industry calls into question the rationality of all sciences.
And in doing so, it brings up an even bigger question: Is science the best path to gaining knowledge in the first place? This is obviously a philosophical question, not a scientific question, and it's beyond the scope of this article, but it's one I will likely visit here on NaturalNews very soon in an upcoming article.
There are many paths to truth, you see. Science -- good science -- is one of them, but it is not the only one. Any scientist who believes that science has a monopoly on all knowledge is himself a fool. Just read a little Feynman and you'll quickly come to discover that the very brightest minds in the history of science consistently recognized there were other pathways leading to truth.
I believe if Feynman were alive today and saw the vaccine propaganda taking place in the name of "science," he would respond with something like, "Surely you're joking."
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• Flu vaccines revealed as the greatest quackery ever pushed in the history of medicine
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About the author: Mike Adams is a consumer health advocate and award-winning journalist with a mission to teach personal and planetary health to the public He has authored more than 1,800 articles and dozens of reports, guides and interviews on natural health topics, impacting the lives of millions of readers around the world who are experiencing phenomenal health benefits from reading his articles.
Adams is an honest, independent journalist and accepts no money or commissions on the third-party products he writes about or the companies he promotes.
In 2010, Adams launched NaturalNews.TV, a natural health video site featuring videos on holistic health and green living. He also founded an environmentally-friendly online retailer called BetterLifeGoods.com that uses retail profits to help support consumer advocacy programs. He's also the CEO of a highly successful email newsletter software company that develops software used to send permission email campaigns to subscribers.
Adams volunteers his time to serve as the executive director of the Consumer Wellness Center, a 501(c)3 non-profit organization, and practices nature photography, Capoeira, martial arts and organic gardening. He's also author of numerous health books published by Truth Publishing and is the creator of several consumer-oriented grassroots campaigns, including the Spam. Don't Buy It! campaign, and the free downloadable Honest Food Guide. He also created the free reference sites HerbReference.com and HealingFoodReference.com.
Adams believes in free speech, free access to nutritional supplements and the ending of corporate control over medicines, genes and seeds. Known as the 'Health Ranger,' Adams' personal health statistics and mission statements are located at www.HealthRanger.org
Our Passion is to reach our individual and collective potential-Always!
Millennium Wellness Enterprises, inc
Wellness can be a profitable enterprise as well people and fit people can continue to be productive, creative and enterprising. Sick people tend to be disabled and lose their productivity over time.
So, it is sound business practice and social practice to stay healthy, well and fit.
Unfortunately, we do not spend time on getting fit, healthy and well as these attributes are not converted into risk management insurance premiums and have value attached to them.
As a result, the medical industry is creating disease via vaccines, to imitate disease and sell the product as beneficial to the unsuspecting public via highly exaggerated scientific credo that has not been yet proven of its benefits.
The scientific tools and models of Risk assessment demand, the pragmatic use of Scientific tools such as Research Pyramid, CORT Analysis, NDSIM, 3As and 3Es and FoC as well as Option Appraisals.
Risk management strategy demands that we under take, Research Pyramid questions of what, why, how, who, when and where to understand the cause and effect relationships. CORT Analysis demands that we look at challenges, opportunities, risks and threats in detail and convert our challenges into opportunities. Most importantly the NDSIM, the Needs, Demands, Supply Interaction Model demands that we look at the question of 3As and 3Es, that is Accessibility, Afford ability, Accountability, in line with Equity, Efficiency and Effectiveness and their delivery in an environment of Freedom of Choice.
Option Appraisal science demands that we look at options and alternatives as well as making choices in the principle of Best Option, Win-Win Option and Compromise Option for an improved opportunity of success.
So, where does vaccine science fall within this bigger picture of empirical science for wellness and optimum health.
It is important to consider wellness science as an alternative to health science, as traditional perspectives have converted health science into sickness science.
The Medical profession is about producing medicines, marketing them and selling them to the public to make profit. However, this does not sound enlightened, so disease and sickness will be through in the mix to make it sound scientific and beneficial to humanity. After all, we are
talking about recovery or the healing profession.
The real science is about staying healthy and well. So, wellness demands pre-emptive fitness and optimum wellness strategy.
All the same it is critical that we appreciate that vaccines should be made accountable to our value system of optimum health and sustainable wellness.
Dr Belai Habte-Jesus
Millennium Wellness Enterprises, Inc
Evidence-based vaccinations: A scientific look at the missing science behind flu season vaccines
Thursday, September 02, 2010
by Mike Adams, the Health Ranger
Editor of NaturalNews.com (See all articles...)
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(NaturalNews) As someone with a good deal of education in scientific thinking and the scientific method, I have put considerable effort into attempting to find any real scientific evidence backing the widespread use of influenza vaccines (flu season shots). Before learning about nutrition and holistic health, I was a computer software entrepreneur, and I have a considerable scientific background in areas such as astronomy, physics, human physiology, microbiology, genetics, anthropology and human psychology. One of my most-admired thought leaders is, in fact, the late physicist Richard Feynman.
I don't speak from a "scientific" point of view on NaturalNews very often because it's often a dry, boring presentation style. But I do know the difference between real science and junk science, and I find examples of junk science in both the "scientific" side of things as well as the "alternative" side of things.
For example, so-called "psychic surgery," as least in the way it has been popularized, is nothing more than clever sleight-of-hand where the surgeon palms some chicken gizzards and then pretends to pull diseased organs out of the abdominal cavity of some patient. The demonstrations I've seen on film are obvious quackery.
Similarly, flu season vaccines are mainstream medicine's version of psychic surgery: It's all just "medical sleight of hand" based on nothing more than clever distractions and the obfuscation of scientific facts. Flu season shots, you see, simply don't work on 99 out of 100 people (and that's being generous to the vaccine industry, as you'll see below).
A year ago, I offered a $10,000 reward to any person who could find scientific proof that H1N1 vaccines were safe and effective (http://www.naturalnews.com/027985_H...). No one even made a claim to collect that reward because no such evidence exists.
Conventional medicine, they say, is really "Evidence-Based Medicine" (EBM). That is, everything promoted by conventional medicine is supposed to be based on "rigorous scientific scrutiny." It's all supposed to be statistically validated and proven beyond a shadow of a doubt that it works as advertised. And in the case of flu vaccines, they are advertised as providing some sort of absolute protection against influenza. "Don't miss work this flu season. Get a flu shot!" The idea, of course, is that getting a flu shot offers 100% protection from the flu. If you get a shot, they say, you won't miss work from sickness.
This implication is wildly inaccurate. In fact, it's just flat-out false. As you'll see below, it's false advertising wrapped around junk science.
You see, there was never an independent, randomized, double-blind, placebo-controlled study proving either the safety or effectiveness of the H1N1 swine flu vaccines that were heavily pushed last year (and are in fact in this year's flu shot cocktail). No such study has ever been done. As a result, there is no rigorous scientific basis from which to sell such vaccines in the first place.
To try to excuse this, vaccine hucksters claim that it would be "unethical" to conduct a placebo-controlled study of such vaccines because they work so well that to deny the placebo group the actual vaccine would be harmful to them. Everybody benefits from the influenza vaccine, they insist, so the mere act of conducting a scientifically-controlled test is unethical.
Do you smell some quackery at work yet? This is precisely the kind of pseudoscientific gobbledygook you might hear from some mad Russian scientist who claims to have "magic water" but you can't test the magic water because the mere presence of measurement instruments nullifies the magical properties of the water.
Similarly, vaccine pushers often insist it's unethical to test whether their vaccines really work. You just have to "take it on faith" that vaccines are universally good for everybody.
Yep, I used the word "faith." That is essentially what the so-called scientific community is invoking here with the vaccine issue: Just BELIEVE they work, everybody! Who needs scientific evidence when we've got FAITH in vaccines?
Forget about evidence-based medicine. Forget about any rational cost-benefit analysis. Forget about the risk-to-benefit ratio calculations that should be part of any rational decision making about vaccines. No, the vaccine industry (and its apologist bloggers) already know that vaccines are universally good for you, therefore no such rigorous scientific assessment is even required!
The Scientific Method, in other words, doesn't really apply to the things they already believe in. Faith can override reason in the "scientific" community, if you can believe that! What's next, are they going to claim vaccines work because some sort of "vaccine God" makes them work?
Here, take your vaccine shot. And don't forget to pray to the Vaccine God because that's how these things really work. Vaccine voodoo, in other words. (Hey, that would have been a great title for the vaccine song, come to think of it...)
Unethical to find out if they work?
I got to wondering about the whole explanation of how it would be "unethical" to test whether the H1N1 vaccines actually work. This deflection strikes me as particularly odd, because it comes with an implied follow-up statement. Here's what they're actually saying when they invoke this excuse:
#1) It is "unethical" to conduct placebo-controlled studies on seasonal flu vaccines to find out if they actually work.
#2) But at the same time, it is entirely ethical to give these shots to hundreds of millions of people, even while lacking any real evidence that they are safe or effective.
In other words, it's unethical to conduct any real science, but entirely ethical to just keep injecting people with a substance that might be entirely useless (or even harmful). That's just a hint of the kind of warped logic and failed ethics that typify our modern vaccine industry.
Vaccine advocates claim that H1N1 vaccines are so effective that NOT giving vaccines to a placebo group would "put their lives at risk." That alone is apparently enough reason to avoid conducting any real science on these vaccines.
But I'm not buying this. I think it's just a cover story -- an excuse to avoid subjecting such vaccines to rigorous scientific inquiry because, deep down inside, they know vaccines would be revealed as an elaborate medical fraud.
So I poked around to see if there were other randomized studies being conducted that might actually put people's lives at risk. It didn't take long to find some. For example, the New England Journal of Medicine recently published two studies regarding post heart-attack patient cooling which seeks to minimize brain damage by physically lowering the temperature of the brain of the heart attack patient until they can reach the acute care technicians at a nearby hospital.
In two studies, researchers who already knew that "cooling" would save lives nevertheless subjected 350 heart attack patient to a randomized study protocol that assigned comatose (but resuscitated) patients to either "cooling" temperatures or normal temperatures.
In one study, while half the cooled patients recovered with normal brain function, only a quarter of those exposed to normal temperatures did. In other words, patient cooling saved their brains. And yet the importance of knowing whether or not this procedure really worked was apparently enough to justify withholding the treatment from over a hundred other patients, most of whom suffered permanent brain damage as a result.
You see, when scientists really want to know the answers to questions like, "Does this brain cooling work?" they have no qualms about subjecting people to things like permanent brain damage in a randomized clinical trial. The knowledge gained from such an experiment is arguably worth the loss of a few patient brains because, armed with scientific evidence, such procedures can be rolled out to help save the brains of potentially hundreds of thousands of patients in subsequent years.
But when it comes to testing vaccines like the recent H1N1 variety, the official explanation is that it's too dangerous to withhold vaccines from a treatment group. They say it's not really important to determine if vaccines are statistically validated, and it's not worth the "risk" of withholding vaccines from anyone in a randomized clinical trial.
Now, sure, there have been some clinical trials done on many different vaccines over the years, but most of those are industry funded, and there are almost never rigorous trials conducted on each year's seasonal flu vaccines before they are released for public consumption. As a result, each year's vaccine is a brand new experiment, carried out across the guinea pig masses of patients who just do whatever they're told without questioning whether it's backed by real science.
Because, of course, it isn't. And I'm not the only one who recognizes this inconvenient fact.
The Cochrane Collaboration
The Cochrane Collaboration, as described on its own website, is, "...an international, independent, not-for-profit organization of over 28,000 contributors from more than 100 countries, dedicated to making up-to-date, accurate information about the effects of health care readily available worldwide."
"We are world leaders in evidence-based health care," the site goes on to say, followed by a quote from The Lancet which states, "The Cochrane Collaboration is an enterprise that rivals the Human Genome Project in its potential implications for modern medicine."
Working for the Cochrane Collaboration, an epidemiologist named Dr. Tom Jefferson decided to take a close look at the scientific evidence behind influenza vaccines (seasonal flu vaccines).
The objectives of the study were to: "Identify, retrieve and assess all studies evaluating the effects of vaccines against influenza in healthy adults."
The Search Criteria: "We searched the Cochrane Central Register of Controlled Trials (CENTRAL) (The Cochrane Library, 2010, issue 2), MEDLINE (January 1966 to June 2010) and EMBASE (1990 to June 2010)."
Selection Criteria (for inclusion in the study): "Randomized controlled trials (RCTs) or quasi-RCTs comparing influenza vaccines with placebo or no intervention in naturally-occurring influenza in healthy individuals aged 16 to 65 years. We also included comparative studies assessing serious and rare harms."
The Total Scope of the study encompassed over 70,000 people. And just so you know, these the results may strongly favor the vaccine industry. The author even went out of his way to warn that "15 out of 36 trials [were] funded by industry (four had no funding declaration)."
In other words, close to half of the studies included in this analysis were funded by the vaccine industry itself, which as we know consistently manipulates data, bribes researchers or otherwise engages in scientific fraud in order to get the results they want.
The author even goes on to warn how industry-funded studies always get more press, saying, "...industry funded studies were published in more prestigious journals and cited more than other studies independently from methodological quality and size."
See the study detail page at: http://onlinelibrary.wiley.com/o/co...
Study results show influenza vaccines are nearly worthless
Now here comes the interesting part: Even though nearly half the studies were funded by the vaccine industry itself, the study results show that in most circumstances, influenza vaccines are virtually worthless:
"The corresponding figures [of people showing influenza symptoms] for poor vaccine matching were 2% and 1% (RD 1, 95% CI 0% to 3%)" say the study authors. And by "poor vaccine matching," they mean that the strain of influenza viruses in the vaccine are a poor match for the strains circulating in the wild. This is usually the case in the real world because the vaccine only incorporates last year's viral strains and cannot predict which strains will be circulating this year.
In other words, you would have to vaccinate 100 people to reduce the number of people showing influenza symptoms by just one. For ninety-nine percent of the people vaccinated, the vaccine makes no difference at all!
In a "best case" scenario when the viral strain in the influenza vaccine just happens to match the strain circulating in the wild -- a situation that even the study authors call "uncommon" -- the results were as follows: "4% of unvaccinated people versus 1% of vaccinated people developed influenza symptoms (risk difference (RD) 3%, 95% confidence interval (CI) 2% to 5%)."
In other words, the matching vaccine (which is uncommon in the real world) reduced influenza infections in 3 out of 100 people. Or, put another way, 97% of those injected with the vaccine received no benefit (and no different outcome).
Furthermore, the study's conclusions go on to state:
• "Vaccination had... no effect on hospital admissions or complication rates."
• "Vaccine use did not affect the number of people hospitalized or working days lost."
• "The review showed that reliable evidence on influenza vaccines is thin but there is evidence of widespread manipulation of conclusions..."
• "There is no evidence that [influenza vaccines] affect complications, such as pneumonia, or transmission." (Got that? Vaccines do not affect transmission of the disease, yet that's the whole reason vaccines are pushed so heavily during pandemics -- to block disease transmission.)
• "In average conditions (partially matching vaccine) 100 people need to be vaccinated to avoid one set of influenza symptoms."
And finally, the study author's summary concludes with this whopper of a statement: "Our results may be an optimistic estimate because company-sponsored influenza vaccines trials tend to produce results favorable to their products and some of the evidence comes from trials carried out in ideal viral circulation and matching conditions and because the harms evidence base is limited."
In other words, taking into account the industry bias, the actual results may be that vaccines prevent influenza symptoms in only 1 out of 1,000 people.
Putting it in perspective
So let's put all this in perspective in a rational, intelligent way. This far-reaching analysis of influenza vaccine trials shows that under common conditions, seasonal influenza vaccines have no benefit for 99 out of 100 people.
Furthermore, even this result is describe as being "an optimistic estimate" because nearly half of the vaccine trials were funded by the vaccine industry which tends to "produce results favorable to their products."
Furthermore, some of the studies were carried out in "ideal" viral matching scenarios that rarely happen in the real world.
And finally, some evidence of harm from vaccines was simply thrown out of this analysis, resulting in a "harms evidence base" that was quite limited and likely doesn't reveal the full picture.
Are you getting all this? Even with industry-funded studies likely distorting the results in their favor, if you take a good hard look at the scientific evidence surrounding the effectiveness of vaccines, you quickly come to realize that influenza vaccines don't work on 99 out of 100 people. (And the real answer may be even worse.)
Now that's a far cry from the false advertising of the vaccine industry, which implies that if you get a shot you're "protected" from influenza. They claim you won't miss work, you'll stay well, and so on. Through these messages, they are cleverly implying that vaccines work on 100% of the people.
But based on the available scientific evidence, these are blatantly false statements. And the wild exaggeration of the supposed benefits from vaccines crosses the threshold of "misleading advertising" and enters the realm of "criminal marketing fraud." Where is the FTC or FDA on speaking out against this quackery?
Vaccine marketing is, essentially, scientific fraud. To claim that vaccines protect everyone when, in reality, they may reduce symptoms in only one out of 100 people is intellectually dishonest and downright fraudulent.
It is, simply put, just pure B.S. quackery.
Now, imagine if an herbal product were advertised on television as offering some health benefit, but it turned out that the product only worked on 1 out of 100 people who took it. That herbal product would be widely branded as "quackery" and the company selling it would be accused of false advertising. The company owners might even be charged with criminal fraud.
But vaccines get a free pass on this issue. While an herbal product might be heavily investigated or even confiscated by the FDA, vaccines that only work on 1% of the people receive the full backing of the FDA, CDC, WHO, FTC and local hospitals and clinics to boot. The fact that the vaccine is pure quackery apparently doesn't matter to any of these organizations: It's full speed ahead, regardless of what the science actually says.
Once you understand all this, you now understand why it is an accurate statement to say "The FDA promotes medical fraud."
Similarly, "The CDC promotes medical fraud." As does the WHO.
These are scientifically accurate statements, assuming you agree that a product that only works on 1 out of 100 people fits the definition of "fraud" when it is marketed as if it helped everyone. And most people would agree with that reasonable definition of fraud.
It's a totally different story if the efficacy ratio is higher. If influenza vaccines actually produced some benefit in 25 out of 100 people, that might be worth considering. But it's nowhere near that.
The FDA, by the way, will often approve pharmaceuticals that only produce results in 5 percent of the clinical trial subjects. The world of modern medicine, in fact, is full of pharmaceuticals that simply don't work on 95% of the patients who take them.
Read the Cochrane summary yourself at:
http://onlinelibrary.wiley.com/o/co...
It's entitled, "Vaccines for preventing influenza in healthy adults"
Authors: "Tom Jefferson, Carlo Di Pietrantonj, Alessandro Rivetti, Ghada A Bawazeer, Lubna A Al-Ansary, Eliana Ferroni"
Enter the vaccine zombies!
With these study results in mind, take a look at some of the lyrics in my recent hip hop song, "Vaccine Zombie" (http://www.naturalnews.com/vaccine_...)
I forgot how to think for myself
I don't understand a thing about health
I do the same as everyone else
I'm a vaccine zombie, zombie
Now you can see where these lyrics come from. If influenza vaccines are worthless for 99 percent of those who receive them, then why are people lining up to get injected?
The answer is because they fail to think critically about vaccines and their health. They don't understand health, so they just go along with everybody else and do what they're told. Hence their earning of the "Vaccine Zombie" designation.
The song goes on to say:
I'm a sucker for the ads, a sucker for the labs
A sucker for the swine flu jabs
and I don't mind followin' a medical fad
Cause livin' without a brain ain't half bad
Yes, people who line up for influenza vaccines are "suckers" who have been bamboozled by fraudulent vaccine propaganda. But they're following a "medical fad" and it's easier to just do what you're told rather than engage your brain and think critically about what you're doing.
"Livin' without a brain ain't half bad" because it takes the burden of decision making out of the loop and allows you to just rely on whatever the doctors and health officials tell you to do.
How the scientific community lost touch with real science
But what if they were all lying to you? Or what if they, themselves, were ignorant about the fact that influenza vaccines are worthless on 99% of those who receive them? (Very few doctors and scientists, it turns out, are aware of this simple truth.)
Or what if the vaccine pushers had all convinced themselves of a falsehood? What if they truly believed that vaccines were really, really good for everyone but that belief was based on wishful thinking rather than rigorous scientific review?
Because that, my friends, is exactly what has happened. We have an entire segment of the scientific community that has been suckered into vaccine propaganda. They've convinced themselves that seasonal flu shots really work and that virtually everyone should be injected with such shots. And they believe this based on irrational faith, not on scientific thinking or rigorous statistical evidence.
They are, in other words, pursuing a vaccine religion (or cult). The is especially curious, given that most vaccine pushers don't believe in God or any organized religion -- except for their own vaccine religion, where real scientific evidence isn't required. All you gotta do is believe in vaccines and you can join their religion, too.
And so all across the 'net, so-called "science bloggers" embarrass themselves by promoting near-useless influenza vaccines as "evidence-based medicine," apparently unaware that the evidence shows such vaccines to be all but worthless.
They might as well say they support vaccines "Just 'cuz."
And "just 'cuz" is no reason to inject yourself with a chemical cocktail that even the industry admits causes extremely dangerous neurological side effects in a small number of vaccine recipients.
Vitamin D would actually make vaccines work better
To top this all off, here's the real kicker of this story: You can beat the minimal protective benefits of vaccines with a simple, low-cost vitamin D supplement. Vitamin D, you see, is the nutrient that activates your immune system to fight off infectious disease. Without it, vaccines hardly work at all.
In fact, the very low rate of vaccine efficacy (1%) is almost certainly due to the fact that most people receiving the vaccines are vitamin D deficient. (Anywhere from 75% - 95% of Americans are deficient in vitamin D, depending on whom you ask.)
Hilariously, the way to make vaccines work better would be to hand out vitamin D supplements to go along with the shots! Even more hilariously, if people were taking vitamin D supplements, they wouldn't need the vaccine shots in the first place!
Influenza vaccines, in other words, have no important role whatsoever in preventing influenza infections. This goal can be accomplished more safely, reliably and at far lower cost by promoting vitamin D supplements for the population at large.
What we really need to see from the scientific world is a study comparing vitamin D supplements to influenza vaccines (and using realistic vitamin D doses, not just 200 or 400 IUs per day). I have absolutely no doubt that healthy-dose vitamin D supplementation (4000 IUs a day) would prove to be significantly more effective than influenza vaccines at preventing flu infections.
But such a study will almost certainly never be done (at least not anytime soon) because it would expose the false propaganda of the vaccine industry while giving consumers a far better way of protecting themselves from influenza that doesn't involve paying money to vaccine manufacturers.
In medicine, as in war, truth is often the first casualty. And when the lies are repeated with enough frequency, they begin to be believed. The flu shot lie has been repeated with such ferocity and apparent authority that it has snookered in virtually the entire "scientific" community.
That even rational-minded scientists can be so easily hoodwinked by the vaccine industry is causing more and more people to question the credibility of not just modern medicine, but the entire scientific community as well.
Because if so-called "rational" scientists and thought leaders can be so easily suckered into an obvious falsehood, what other fictions might they be promoting as fact?
Medicine, you see, makes all the other sciences look bad. The obvious scientific fraud going on in the name of "science" in the pharmaceutical industry makes a mockery of real scientific thought. The ease of which medical scientists have been hoodwinked by the drug industry calls into question the rationality of all sciences.
And in doing so, it brings up an even bigger question: Is science the best path to gaining knowledge in the first place? This is obviously a philosophical question, not a scientific question, and it's beyond the scope of this article, but it's one I will likely visit here on NaturalNews very soon in an upcoming article.
There are many paths to truth, you see. Science -- good science -- is one of them, but it is not the only one. Any scientist who believes that science has a monopoly on all knowledge is himself a fool. Just read a little Feynman and you'll quickly come to discover that the very brightest minds in the history of science consistently recognized there were other pathways leading to truth.
I believe if Feynman were alive today and saw the vaccine propaganda taking place in the name of "science," he would respond with something like, "Surely you're joking."
Articles Related to This Article:
• Facebook crowdsourced investigation exposes vaccine denials of SIGA Technologies
• The great thimerosal cover-up: Mercury, vaccines, autism and your child's health
• Flu vaccines revealed as the greatest quackery ever pushed in the history of medicine
• Vaccines cause autism: Supporting evidence
• Are mandatory vaccinations acts of violence against children?
• Ten questions about flu vaccines that doctors and health authorities refuse to answer
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About the author: Mike Adams is a consumer health advocate and award-winning journalist with a mission to teach personal and planetary health to the public He has authored more than 1,800 articles and dozens of reports, guides and interviews on natural health topics, impacting the lives of millions of readers around the world who are experiencing phenomenal health benefits from reading his articles.
Adams is an honest, independent journalist and accepts no money or commissions on the third-party products he writes about or the companies he promotes.
In 2010, Adams launched NaturalNews.TV, a natural health video site featuring videos on holistic health and green living. He also founded an environmentally-friendly online retailer called BetterLifeGoods.com that uses retail profits to help support consumer advocacy programs. He's also the CEO of a highly successful email newsletter software company that develops software used to send permission email campaigns to subscribers.
Adams volunteers his time to serve as the executive director of the Consumer Wellness Center, a 501(c)3 non-profit organization, and practices nature photography, Capoeira, martial arts and organic gardening. He's also author of numerous health books published by Truth Publishing and is the creator of several consumer-oriented grassroots campaigns, including the Spam. Don't Buy It! campaign, and the free downloadable Honest Food Guide. He also created the free reference sites HerbReference.com and HealingFoodReference.com.
Adams believes in free speech, free access to nutritional supplements and the ending of corporate control over medicines, genes and seeds. Known as the 'Health Ranger,' Adams' personal health statistics and mission statements are located at www.HealthRanger.org
Connecting our humanity via geneology even when we have to fight to survive
Global7 the new Millennial Renaissance Vision for the Globe
Obama Distant Kin to Palin, Limbaugh, Bush, Ancestry.com Says
By Traci McMillan - Oct 13, 2010 12:01 AM ET
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U.S. President Barack Obama speaking in Washington. Photographer: Joshua Roberts/Bloomberg
Sarah Palin, former governor of Alaska and 2008 vice presidential candidate, attending the Southern Republican Leadership Conference in New Orleans. Photographer: Patrick Semansky/Bloomberg
President Barack Obama is distantly related to two of his most outspoken critics -- Tea Party favorite Sarah Palin and talk-radio host Rush Limbaugh -- as well as to former President George W. Bush, according to a genealogy website.
Family trees revealed Obama and Palin, the former Alaska Governor and 2008 Republican vice presidential nominee, are 10th cousins through common ancestor John Smith, according to Ancestry.com Inc. Smith was Obama’s and Palin’s 12th-great- grandfather. Smith, a Protestant pastor, was an early settler in Massachusetts and was criticized by the ecclesiastical community for supporting Quakers, said Anastasia Tyler, a genealogist for the website.
Obama and Limbaugh are 10th cousins once removed through shared connections to Richmond Terrell, a Virginia settler who came to America in the mid-1600s, Tyler said.
Palin and Obama have ties to Bush, both through links to Samuel Hinckley. Maybe leadership “runs in the family,” the website said, because Hinckley’s son, Thomas, became the governor of Plymouth Colony before it united with Massachusetts.
“Despite political differences, they do have similarities,” Tyler said. “We are all tied together; we are all part of America.”
The family-tree website also found that Palin is related to U.S. Senate Majority Leader Harry Reid, a Nevada Democrat, and author and commentator Ann Coulter. The three are tied to John Lathrop, an Englishman who was banished to Boston after he served as minister of an illegal church independent of the Church of England, Tyler said.
Family Trees
Tyler’s team at Provo, Utah-based Ancestry.com works on discovering famous relations to show how people can build family trees from the site, using its library of 5 billion historical records.
“We are always looking for ways to show how interesting family history can be,” Tyler said.
The site has previously linked Obama to billionaire Warren Buffett and actor Brad Pitt. It also found family ties between Palin and Princess Diana.
To contact the reporter on this story: Traci McMillan in Washington at tmcmillan1@bloomberg.net
To contact the editor responsible for this story: Mark Silva in Washington at msilva34@bloomberg.net.
Obama Distant Kin to Palin, Limbaugh, Bush, Ancestry.com Says
By Traci McMillan - Oct 13, 2010 12:01 AM ET
Tweet (40) LinkedIn Share Print Email
U.S. President Barack Obama speaking in Washington. Photographer: Joshua Roberts/Bloomberg
Sarah Palin, former governor of Alaska and 2008 vice presidential candidate, attending the Southern Republican Leadership Conference in New Orleans. Photographer: Patrick Semansky/Bloomberg
President Barack Obama is distantly related to two of his most outspoken critics -- Tea Party favorite Sarah Palin and talk-radio host Rush Limbaugh -- as well as to former President George W. Bush, according to a genealogy website.
Family trees revealed Obama and Palin, the former Alaska Governor and 2008 Republican vice presidential nominee, are 10th cousins through common ancestor John Smith, according to Ancestry.com Inc. Smith was Obama’s and Palin’s 12th-great- grandfather. Smith, a Protestant pastor, was an early settler in Massachusetts and was criticized by the ecclesiastical community for supporting Quakers, said Anastasia Tyler, a genealogist for the website.
Obama and Limbaugh are 10th cousins once removed through shared connections to Richmond Terrell, a Virginia settler who came to America in the mid-1600s, Tyler said.
Palin and Obama have ties to Bush, both through links to Samuel Hinckley. Maybe leadership “runs in the family,” the website said, because Hinckley’s son, Thomas, became the governor of Plymouth Colony before it united with Massachusetts.
“Despite political differences, they do have similarities,” Tyler said. “We are all tied together; we are all part of America.”
The family-tree website also found that Palin is related to U.S. Senate Majority Leader Harry Reid, a Nevada Democrat, and author and commentator Ann Coulter. The three are tied to John Lathrop, an Englishman who was banished to Boston after he served as minister of an illegal church independent of the Church of England, Tyler said.
Family Trees
Tyler’s team at Provo, Utah-based Ancestry.com works on discovering famous relations to show how people can build family trees from the site, using its library of 5 billion historical records.
“We are always looking for ways to show how interesting family history can be,” Tyler said.
The site has previously linked Obama to billionaire Warren Buffett and actor Brad Pitt. It also found family ties between Palin and Princess Diana.
To contact the reporter on this story: Traci McMillan in Washington at tmcmillan1@bloomberg.net
To contact the editor responsible for this story: Mark Silva in Washington at msilva34@bloomberg.net.
Tuesday, October 05, 2010
Nobel Prize for Medicine goes to Invitro Fertilization Scientists
Global7 the new Millennial Renaissance Vision for the Globe
Our Passion is to reach our individual and collective potential 4 Excellence & Success!
IVF doctors, families celebrate creator's Nobel Prize
By Elizabeth Landau and Jamie Gumbrecht, CNN
October 4, 2010 6:43 p.m. EDT
Brendan Harley and his wife, Kathryn Clancy, had their daughter, Joan, through in vitro fertilization.
STORY HIGHLIGHTS
In vitro fertilization, once controversial, is practically an everyday procedure today
About 1 percent of infants born in U.S. are conceived through assisted reproduction
High cost of in vitro is still prohibitive for many couples
Next goal is to improve the success rate, reduce multiple births
(CNN) -- Brendan Harley beat cancer once as an infant, then faced leukemia as a teen. He survived, but the illnesses left him infertile and feeling guilty.
"He knew that I wanted children and was excited to have children, and I think he was sad that he was complicating things," said Harley's wife, Kathryn Clancy, 31. "But if anything, I feel like things just worked out so wonderfully that there was just no need to be upset."
Clancy and Harley, both assistant professors at the University of Illinois, now have a 2 ½-year-old daughter, Joan. She was conceived through in vitro fertilization, a technology that involves combining sperm and egg outside the body and implanting the resulting embryos.
"You look at this child and you think, 'How could my life be any different?' I can't imagine how sad I'd be if this wasn't how my life looked right now," said Clancy, a biological anthropologist.
Just a few decades ago, the technology that allowed Joan to be born didn't exist. One of its creators, Robert G. Edwards, won the Nobel Prize for medicine on Monday. Many families and doctors said it's a well-earned prize that brought precious lives into the world.
Share your 'test-tube baby' story: Send an iReport
"Bob Edwards certainly made a major impact on what we do we do every day, and the four million babies born as a result," said Dr. James Goldfarb, president of the Society for Assisted Reproductive Technology and director of infertility services at the Cleveland Clinic Health Systems.
In vitro fertilization technology has evolved since the first successful birth in 1978, Goldfarb said, but he uses another word to describe the work of Edwards and his partner, Dr. Patrick Steptoe, who died in 1988: Revolution.
Robert G. Edwards wins Nobel Prize
Today, about 1 percent of infants born in the United States are conceived through assisted reproductive technologies, and 99 percent of those use in vitro fertilization, the U.S. Department of Health and Human Services reported in 2009. It's a medical procedure the public knows, doctors said, and infertile couples expect for it to be on the list of treatments.
They're well-aware that since 1978, miracles have been possible.
Controversial births
The first baby ever born through IVF was Louise Joy Brown, delivered through a Caesarean section on July 25, 1978, at a hospital in England. She gave birth to a son in 2006.
Elizabeth Comeau, born Elizabeth Jordan Carr in 1981, was the first so-called "test tube baby" in the United States, and recently had a child of her own.
Dr. Dorothy Mitchell-Leef, a fertility specialist in private practice in Atlanta, Georgia, remembers the buzz surrounding Brown's birth at the American Society of Reproductive Medicine meeting shortly after.
"It was extremely exciting to hear about it and know that it could be achieved," she said.
Early on, Edwards' and Steptoe's work on in vitro fertilization met opposition from some government officials, who were concerned with potential overpopulation, and some religious groups. Catholic church leaders have long opposed in vitro fertilization because, they said, it depersonalizes conception and disposes of some embryos, which they argue is the equivalent to abortion.
Doctors remember protesters at medical conventions and fertility clinics that struggled to stay open. Now, they said, curiosity and science fiction-style reporting have calmed. Families celebrate unlikely births, schools might have multiple sets of twins and triplets and the first babies born through in vitro fertilization are having their own babies the natural way.
"I don't think it's a stigma to parents or the child," said Dr. Louis DePaolo, chief of the National Institute of Child Health and Human Development's Reproductive Sciences Branch. "There are couples who go through hell, the stress of infertility and going through these treatments. There's no question [why they do it] -- the desire to have a family."
A costly procedure
The barrier for many couples now is cost. One round of in vitro fertilization can cost about $15,000. Many insurance policies don't cover it, and some couples require more than one attempt.
Kathryn Clancy's child, Joan, was born through a procedure that combined Clancy's egg with the sperm from one of Harley's brothers. Harley's other brother had been a bone marrow donor when he had leukemia at 17.
Clancy and Harley met with a fertility specialist in January 2007. The following six months were a mix of paperwork, testing, hormones and medications to prepare Clancy's body for the embryo transfer. The process of injecting herself frightened Clancy, so her husband did it for her the first week; cancer had made him comfortable with needles.
The first trimester was scariest, Clancy said. Early on, she had cramps and fears of a miscarriage. But the process worked on the first try, with a single embryo.
Joan Adele Clancy-Harley was born after a natural labor at a midwife-attended birth center in Massachusetts. It was a "textbook" pregnancy and a nonmedical end to an intense medical experience, Clancy noted.
Next challenges
Those are the types of fertility stories doctors like.
The in vitro process has been simplified to ease the initial removal of a woman's eggs, to help men with low numbers of sperm and to use the most viable embryos. Long-term studies have shown that children born as a result of in vitro fertilization are as healthy as children born after natural conception. Still, not all attempts are successful and not all pregnancies go smoothly.
Some doctors transfer more than one embryo to improve chances of a pregnancy, but multiple births can lead to greater risks during pregnancy and after delivery. Widespread attention to Nadya Suleman, the mother of octuplets born in California in 2009, has led to more discussions about ethics and limits of in vitro fertilization.
Doctors say the goals now are to improve the success rate, especially for older parents, while reducing the number of multiple births. Then there's the bigger question: How to prevent or treat infertility altogether?
"We're bypassing. The couples are still infertile," DePaolo said. "We need to pursue the root causes of infertility and have better treatments, and ameliorate the major reasons to need in vitro fertilization."
That, they said, could be the work of future Nobel Prize.
CNN's Madison Park contributed to this report.
We recommend
Children of divorce vow to break cycle, create enduring marriages
Doctor sued for 'branding' patient's uterus
Sarandon didn't expect her, Robbins to split
Are once-happy boomers behind rise in midlife suicide?
Vatican official criticizes award of Nobel Prize to Robert Edwards
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Our Passion is to reach our individual and collective potential 4 Excellence & Success!
IVF doctors, families celebrate creator's Nobel Prize
By Elizabeth Landau and Jamie Gumbrecht, CNN
October 4, 2010 6:43 p.m. EDT
Brendan Harley and his wife, Kathryn Clancy, had their daughter, Joan, through in vitro fertilization.
STORY HIGHLIGHTS
In vitro fertilization, once controversial, is practically an everyday procedure today
About 1 percent of infants born in U.S. are conceived through assisted reproduction
High cost of in vitro is still prohibitive for many couples
Next goal is to improve the success rate, reduce multiple births
(CNN) -- Brendan Harley beat cancer once as an infant, then faced leukemia as a teen. He survived, but the illnesses left him infertile and feeling guilty.
"He knew that I wanted children and was excited to have children, and I think he was sad that he was complicating things," said Harley's wife, Kathryn Clancy, 31. "But if anything, I feel like things just worked out so wonderfully that there was just no need to be upset."
Clancy and Harley, both assistant professors at the University of Illinois, now have a 2 ½-year-old daughter, Joan. She was conceived through in vitro fertilization, a technology that involves combining sperm and egg outside the body and implanting the resulting embryos.
"You look at this child and you think, 'How could my life be any different?' I can't imagine how sad I'd be if this wasn't how my life looked right now," said Clancy, a biological anthropologist.
Just a few decades ago, the technology that allowed Joan to be born didn't exist. One of its creators, Robert G. Edwards, won the Nobel Prize for medicine on Monday. Many families and doctors said it's a well-earned prize that brought precious lives into the world.
Share your 'test-tube baby' story: Send an iReport
"Bob Edwards certainly made a major impact on what we do we do every day, and the four million babies born as a result," said Dr. James Goldfarb, president of the Society for Assisted Reproductive Technology and director of infertility services at the Cleveland Clinic Health Systems.
In vitro fertilization technology has evolved since the first successful birth in 1978, Goldfarb said, but he uses another word to describe the work of Edwards and his partner, Dr. Patrick Steptoe, who died in 1988: Revolution.
Robert G. Edwards wins Nobel Prize
Today, about 1 percent of infants born in the United States are conceived through assisted reproductive technologies, and 99 percent of those use in vitro fertilization, the U.S. Department of Health and Human Services reported in 2009. It's a medical procedure the public knows, doctors said, and infertile couples expect for it to be on the list of treatments.
They're well-aware that since 1978, miracles have been possible.
Controversial births
The first baby ever born through IVF was Louise Joy Brown, delivered through a Caesarean section on July 25, 1978, at a hospital in England. She gave birth to a son in 2006.
Elizabeth Comeau, born Elizabeth Jordan Carr in 1981, was the first so-called "test tube baby" in the United States, and recently had a child of her own.
Dr. Dorothy Mitchell-Leef, a fertility specialist in private practice in Atlanta, Georgia, remembers the buzz surrounding Brown's birth at the American Society of Reproductive Medicine meeting shortly after.
"It was extremely exciting to hear about it and know that it could be achieved," she said.
Early on, Edwards' and Steptoe's work on in vitro fertilization met opposition from some government officials, who were concerned with potential overpopulation, and some religious groups. Catholic church leaders have long opposed in vitro fertilization because, they said, it depersonalizes conception and disposes of some embryos, which they argue is the equivalent to abortion.
Doctors remember protesters at medical conventions and fertility clinics that struggled to stay open. Now, they said, curiosity and science fiction-style reporting have calmed. Families celebrate unlikely births, schools might have multiple sets of twins and triplets and the first babies born through in vitro fertilization are having their own babies the natural way.
"I don't think it's a stigma to parents or the child," said Dr. Louis DePaolo, chief of the National Institute of Child Health and Human Development's Reproductive Sciences Branch. "There are couples who go through hell, the stress of infertility and going through these treatments. There's no question [why they do it] -- the desire to have a family."
A costly procedure
The barrier for many couples now is cost. One round of in vitro fertilization can cost about $15,000. Many insurance policies don't cover it, and some couples require more than one attempt.
Kathryn Clancy's child, Joan, was born through a procedure that combined Clancy's egg with the sperm from one of Harley's brothers. Harley's other brother had been a bone marrow donor when he had leukemia at 17.
Clancy and Harley met with a fertility specialist in January 2007. The following six months were a mix of paperwork, testing, hormones and medications to prepare Clancy's body for the embryo transfer. The process of injecting herself frightened Clancy, so her husband did it for her the first week; cancer had made him comfortable with needles.
The first trimester was scariest, Clancy said. Early on, she had cramps and fears of a miscarriage. But the process worked on the first try, with a single embryo.
Joan Adele Clancy-Harley was born after a natural labor at a midwife-attended birth center in Massachusetts. It was a "textbook" pregnancy and a nonmedical end to an intense medical experience, Clancy noted.
Next challenges
Those are the types of fertility stories doctors like.
The in vitro process has been simplified to ease the initial removal of a woman's eggs, to help men with low numbers of sperm and to use the most viable embryos. Long-term studies have shown that children born as a result of in vitro fertilization are as healthy as children born after natural conception. Still, not all attempts are successful and not all pregnancies go smoothly.
Some doctors transfer more than one embryo to improve chances of a pregnancy, but multiple births can lead to greater risks during pregnancy and after delivery. Widespread attention to Nadya Suleman, the mother of octuplets born in California in 2009, has led to more discussions about ethics and limits of in vitro fertilization.
Doctors say the goals now are to improve the success rate, especially for older parents, while reducing the number of multiple births. Then there's the bigger question: How to prevent or treat infertility altogether?
"We're bypassing. The couples are still infertile," DePaolo said. "We need to pursue the root causes of infertility and have better treatments, and ameliorate the major reasons to need in vitro fertilization."
That, they said, could be the work of future Nobel Prize.
CNN's Madison Park contributed to this report.
We recommend
Children of divorce vow to break cycle, create enduring marriages
Doctor sued for 'branding' patient's uterus
Sarandon didn't expect her, Robbins to split
Are once-happy boomers behind rise in midlife suicide?
Vatican official criticizes award of Nobel Prize to Robert Edwards
From around the web
Bipolar Is One Disorder With Many Faces Health.com
Humalin N HealthGuru.com
Early Signs That You Might Have Multiple Sclerosis EverydayHealth.com
10 Celebrities Talk About Their Depression The Frisky
Why Fibromyalgia Has a Credibility Problem Health.com
Thursday, September 23, 2010
Understanding Stroke or Cerebrovascular Accidents
Global7 the new Millennial Renaissance Vision for the Globe
Stroke (CVA)-
Update and Revision s
Introduction
A stroke occurs when an artery to the brain becomes blocked or ruptures, resulting in death of an area of brain tissue (cerebral infarction) and causing sudden symptoms.
1. Most strokes are ischemic (usually due to blockage of an artery), but some are hemorrhagic (due to rupture of an artery).
2. Transient ischemic attacks resemble ischemic strokes except the symptoms resolve within 1 hour.
3. Symptoms occur suddenly and can include muscle weakness, paralysis, abnormal or lost sensation on one side of the body, difficulty speaking, confusion, problems with vision, dizziness, and loss of balance and coordination.
4. Diagnosis is based on symptoms, but imaging and blood tests are also done.
5. Recovery after a stroke depends on many factors, such the location and amount of damage, the person's age, and the presence of other disorders.
6. Controlling high blood pressure, high cholesterol levels, and high blood sugar levels and not smoking help prevent strokes.
7. Treatment may include drugs to make blood less likely to clot or to break up clots and sometimes surgery.
A stroke is called a cerebrovascular disorder because it affects the brain (cerebro-) and the blood vessels (vascular).
Supplying the Brain With Blood
Blood is supplied to the brain through two pairs of large arteries:
• Internal carotid arteries, which carry blood from the heart along the front of the neck
• Vertebral arteries, which carry blood from the heart along the back of the neck
Understanding the Pato- physiology of stroke
In the skull, the vertebral arteries unite to form the basilar artery (at the back of the head). The internal carotid arteries and the basilar artery divide into several branches, including the cerebral arteries. Some branches join to form a circle of arteries (circle of Willis) that connect the vertebral and internal carotid arteries. Other arteries branch off from the circle of Willis like roads from a traffic circle. The branches carry blood to all parts of the brain.
When the large arteries that supply the brain are blocked, some people have no symptoms or have only a small stroke. But others with the same sort of blockage have a massive ischemic stroke. Why? Part of the explanation is collateral arteries. Collateral arteries run between other arteries, providing extra connections.
Cerebral Arteries
These arteries include the circle of Willis and connections between the arteries that branch off from the circle. Some people are born with large collateral arteries, which can protect them from strokes. Then when one artery is blocked, blood flow continues through a collateral artery, sometimes preventing a stroke. Other people are born with small collateral arteries. Small collateral arteries may be unable to pass enough blood to the affected area, so a stroke results.
Protection against stroke
The body can also protect itself against strokes by growing new arteries. When blockages develop slowly and gradually (as occurs in atherosclerosis), new arteries may grow in time to keep the affected area of the brain supplied with blood and thus prevent a stroke. If a stroke has already occurred, growing new arteries can help prevent a second stroke (but cannot reverse damage that has been done).
Epidemiology
In Western countries, strokes are the third most common cause of death and the most common cause of disabling neurologic damage. In the United States, over 600,000 people have a stroke and about 160,000 die of stroke each year.
Older people
Strokes are much more common among older people than among younger adults, usually because the disorders that lead to strokes progress over time. Over two thirds of all strokes occur in people older than 65. Slightly more than 50% of all strokes occur in men, but more than 60% of deaths due to stroke occur in women, possibly because women are on average older when the stroke occurs. Blacks are more likely than whites to have a stroke and to die of it.
Types of Stroke (Ischemic 80%; and hemorrhagic, 20%)
Types: There are two types of strokes: ischemic and hemorrhagic. About 80% of strokes are ischemic—usually due to a blocked artery, often blocked by a blood clot. Brain cells, thus deprived of their blood supply, do not receive enough oxygen and glucose (a sugar), which are carried by blood.
Oxygen deprivation
The damage that results depends on how long brain cells are deprived of blood. If they are deprived for only a brief time, brain cells are stressed, but they may recover. If brain cells are deprived longer (but possibly for only several minutes), brain cells die, and some functions may be lost. However, in such cases, a different area of the brain can sometimes learn how to do the functions previously done by the damaged area.
Transient Ischemic Attacks (TIAs) - Ministrokes
Transient ischemic attacks (TIAs), sometimes called ministrokes, are often an early warning sign of an impending ischemic stroke. They are caused by a brief interruption of the blood supply to part of the brain. Because the blood supply is restored quickly, brain tissue may not die, as it does in a stroke
Hemorrhagic strokes..
The other 20% of strokes are hemorrhagic—due to bleeding in or around the brain. In this type of stroke, a blood vessel ruptures, interfering with normal blood flow and allowing blood to leak into brain tissue. Blood that comes into direct contact with brain tissue irritates the tissue and can cause scarring, leading to seizures.
Risk Factors: The major risk factors for both types of stroke are
1. Atherosclerosis (narrowing or blockage of arteries by patchy deposits of fatty material in the walls of arteries)
2. High cholesterol levels
3. High blood pressure
4. Diabetes
5. Smoking
Atherosclerosis is a more important risk factor for ischemic stroke, and high blood pressure is a more important risk factor for hemorrhagic stroke. These risk factors can be controlled to some extent.
Other risk factors include
1. Having relatives who have had a stroke
2. Consuming too much alcohol
3. Using cocaine or amphetamines
4. Having an abnormal heart rhythm called atrial fibrillation
5. Having inflamed blood vessels (vasculitis)
For hemorrhagic stroke, risk factors also include using anticoagulants, having a bulge (aneurysm) in arteries within the skull, and having an abnormal connection between arteries and veins (arteriovenous malformation).
Incidence
The incidence of strokes has declined in recent decades, mainly because people are more aware of the importance of controlling high blood pressure and high cholesterol levels and stopping cigarette smoking. Controlling these factors reduces the risk of atherosclerosis.
Symptoms
Symptoms of a stroke or transient ischemic attack occur suddenly. They vary depending on the precise location of the blockage or bleeding in the brain (Brain Dysfunction: Dysfunction by Location and Brain Dysfunction: When Specific Areas of the Brain Are Damaged ).
Each area of the brain is supplied by specific arteries. For example, if an artery supplying the area of the brain that controls the left leg's muscle movements is blocked, the leg becomes weak or paralyzed. If the area of the brain that senses touch in the right arm is damaged, sensation in the right arm is lost.
Early treatment
Because early treatment can help limit loss of function and sensation, everyone should know what the early symptoms of stroke are. People who have any of these symptoms should see a doctor immediately, even if the symptom goes away quickly.
Most strokes, whether ischemic or hemorrhagic, typically cause one or more of the following symptoms:
1. Sudden weakness or paralysis on one side of the body (for example, half of the face, one arm or leg, or all of one side)
2. Sudden loss of sensation or abnormal sensations on one side of the body
3. Sudden difficulty speaking, sometimes with slurred speech
4. Sudden confusion, with difficulty understanding speech
5. Sudden dimness, blurring, or loss of vision, particularly in one eye
6. Sudden dizziness or loss of balance and coordination, leading to falls
Symptoms of a transient ischemic attack are the same, but they usually disappear within minutes and rarely last more than 1 hour.
Why Strokes Affect Only One Side of the Body
Strokes usually damage only one side of the brain. Because nerves in the brain cross over to the other side of the body, symptoms appear on the side of the body opposite the damaged side of the brain.
Symptoms of a hemorrhagic stroke may also include the following:
1. Sudden severe headache
2. Nausea and vomiting
3. Temporary or persistent loss of consciousness
4. Very high blood pressure
Other symptoms that may occur early include problems with memory, thinking, attention, or learning. People may be unable to recognize parts of the body and may be unaware of the stroke's effects. The peripheral field of vision may be reduced, and hearing may be partially lost.
Dizziness and vertigo may develop or persist. Control of bowel or bladder function may be lost.
Later symptoms may include stiffening and spasms of the muscles (spasticity) and inability to control emotions. A stroke can cause depression, or people may feel depressed because of the stroke.
In most people who have had an ischemic stroke, loss of function is usually greatest immediately after the stroke occurs. However, in about 15 to 20%, the stroke is progressive, causing greatest loss of function after a day or two. In people who have had a hemorrhagic stroke, function usually is lost progressively over minutes to hours.
Over days to months, some function is usually regained because even though some brain cells die, others are only stressed and may recover. Also, certain areas of the brain can sometimes switch to the functions previously done by the damaged part—a characteristic called plasticity. However, the early effects of a stroke, including paralysis, can become permanent. Muscles that are not used usually become permanently spastic and stiff, and painful muscle spasms may occur.
Walking, swallowing, physically saying words clearly, and doing daily activities may remain difficult.
Various problems with memory, thinking, attention, learning, or controlling emotions may persist. Depression, impairments in hearing or vision, or vertigo may be continuing problems. Control of bowel or bladder function may be permanently impaired.
Complications: When a stroke is severe, the brain swells, increasing pressure within the skull. Increased pressure can damage the brain directly or indirectly by forcing the brain downward in the skull.
The brain may be forced through the rigid structures that separate the brain into compartments, resulting in a serious problem called herniation (see Head Injuries:Introduction ). The pressure affects the respiratory center in the lower part of the brain stem and can cause irregular breathing, loss of consciousness, coma, and death.
The symptoms caused by a stroke can lead to other problems. If swallowing is difficult, people may inhale food, fluids, or other particles from the mouth. Such inhalation (called aspiration) can cause aspiration pneumonia, which may be serious.
Difficulty swallowing can also interfere with eating, resulting in under nutrition and dehydration. Not being able to move can result in pressure sores, muscle loss, and the formation of blood clots in deep veins of the legs and groin (deep vein thrombosis). Clots can break off, travel through the bloodstream, and block an artery to a lung (pulmonary embolism). If bladder control is impaired, urinary tract infections are more likely to develop.
Diagnosis
Symptoms suggest the diagnosis, but tests are needed to help doctors determine the following:
1. Whether stroke has occurred
2. Whether it is ischemic or hemorrhagic
3. Whether immediate treatment is required
Computed tomography (CT–see Common Imaging Tests: Computed Tomography) or magnetic resonance imaging (MRI–see Common Imaging Tests: Magnetic Resonance Imaging) of the brain is done. These tests can detect most hemorrhagic strokes, except for some subarachnoid hemorrhages. These tests can also detect many ischemic strokes but sometimes not until several hours after symptoms appear. The blood sugar level is measured immediately because a low blood sugar level (hypoglycemia) can cause symptoms similar to those of stroke.
Doctors evaluate people who have had a stroke for problems that can contribute to or cause a stroke, such as infection, a low blood oxygen level, and dehydration, Tests are done as needed.
People are asked about depression. The ability to swallow is evaluated, sometimes with x-rays taken after a radiopaque dye such as barium is swallowed. Depending on the type of stroke, more tests are done to identify the cause.
Prognosis
Certain factors suggest that the outcome of a stroke is likely to be poor. Strokes that cause unconsciousness or that affect a large part of the left side of the brain (which is responsible for language) may be particularly grave.
In adults who have had an ischemic stroke, problems that remain after 6 months are likely to be permanent, but children continue to improve slowly for many months. Older people fare less well than younger people. For people who already have other serious disorders (such as dementia), recovery is more limited.
If a hemorrhagic stroke is not massive and pressure within the brain is not very high, the outcome is likely to be better after than that after an ischemic stroke. Blood (in a hemorrhagic stroke) does not damage brain tissue as much as an inadequate supply of oxygen (in an ischemic stroke) does.
Prevention
Preventing strokes is preferable to treating them. The main strategy for preventing a first stroke is managing the major risk factors. High blood pressure (see High Blood Pressure) and diabetes (see Diabetes Mellitus (DM): Diabetes Mellitus)should be controlled. Cholesterol levels should be measured and, if high, lowered to reduce the risk of atherosclerosis (see Cholesterol Disorders: Treatment).
Smoking and use of amphetamines or cocaine should be stopped, and alcohol should be limited to no more than 2 drinks a day. Exercising regularly and, if overweight, losing weight help people control high blood pressure, diabetes, and high cholesterol levels. Having regular checkups enables a doctor to identify risk factors for stroke so that they can be managed quickly.
If people have had an ischemic stroke, taking an antiplatelet drug can reduce the risk of another ischemic stroke. Antiplatelet drugs make platelets less likely to clump and form clots, a common cause of ischemic stroke. (Platelets are tiny cell-like particles in blood that help it clot in response to damaged blood vessels.)
Aspirin , one of the most effective antiplatelet drugs, is usually prescribed. One adult's tablet or 1 children's tablet (which is about one fourth the dose of an adult aspirin ) is taken each day. Either dose seems to prevent strokes about equally well.
Taking a combination tablet that contains a low dose of aspirin and dipyridamole (an antiplatelet drug) is slightly more effective than taking aspirin alone.
Clopidogrel , another antiplatelet drug, is also slightly more effective than aspirin alone. It may be given to people who cannot tolerate aspirin.
Some people are allergic to antiplatelet drugs or similar drugs and cannot take them. Also, people who have gastrointestinal bleeding should not take antiplatelet drugs.
If an ischemic stroke or a transient ischemic attack is due to blood clots originating in the heart, warfarin , an anticoagulant, may be given to inhibit blood clotting. Because taking warfarin and an antiplatelet drug or taking aspirin plus clopidogrel greatly increases the risk of bleeding, these drugs are rarely used together for stroke prevention.
Treatment
Anyone with symptoms of a stroke should seek medical attention immediately.
Doctors check the person's vital functions, such as heart rate, breathing, temperature, and blood pressure, to make sure they are adequate. If they are not, measures to correct them are taken immediately.
For example, if people are in a coma or unresponsive (as may result from brain herniation), mechanical ventilation (with a breathing tube inserted through the mouth or nose) may be needed to help them breathe.
If symptoms suggest that pressure within the skull is high, drugs may be given to reduce swelling in the brain, and a monitor may be put in the brain to periodically measure the pressure.
Other treatments used during the first hours depend on the type of stroke. These treatments include drugs (such as antiplatelet drugs, anticoagulants, drugs to break up clots, and drugs to control high blood pressure) and surgery to remove blood that has accumulated.
Later and ongoing treatments focus on preventing subsequent strokes, treating and preventing problems that strokes can cause, and helping people regain as much function as possible (rehabilitation).
Preventing and Treating Problems After a Stroke
Problem Measures
Blood clots in the legs To prevent blood clots, doctors may give anticoagulants, such as heparin or low molecular weight heparin, put elastic or air-filled support stockings on the person's legs to improve blood circulation, or both.Moving the legs, which improves blood flow, can also help. People, if able, are encouraged to walk or simply move their legs (for example, extending and flexing their ankles). If people cannot move their legs, a therapist or other staff member moves their legs for them (called passive exercise).
Pressure sores Nurses, other staff members, or caregivers should frequently turn or reposition people who are confined to a bed or wheelchair. Areas likely to develop pressures sores should be inspected every day.
Permanent shortening of muscles that limits movement (contractures) Moving the limbs can prevent contractures. People, if able, are encouraged to move and change positions regularly. Or a therapist or other staff member moves their limbs for them and makes sure the limbs are placed in appropriate resting positions. Sometimes splints are used to keep the limbs in place.
Difficulty swallowing People are evaluated for difficulty swallowing. If they have difficulty, care is taken to provide them with enough fluids and nourishment. Sometimes learning simple techniques (for example, how to position the head, how to breathe when swallowing) can help the person swallow safely. Tube feedings may be necessary until the ability to swallow returns.
Difficulty breathing If people smoke, they are encouraged to stop. Therapists also teach them to do deep breathing exercises and to cough to clear the airways. Therapists may provide a handheld breathing device. If needed, oxygen is provided through a face mask or a tube inserted in the nose or in the mouth.
Urinary tract infections If possible, a urinary catheter, which can cause urinary infections, is not used. If a catheter is needed, it is removed as soon as possible.
Discouragement and depression Doctors discuss the effects of the stroke with affected people and their family members or other caregivers. The discussion includes the type of recovery that can be expected and ways to cope with limitations of function. People and their caregivers are put in contact with stroke support groups. Formal counseling or drugs may be necessary to treat depression.
Rehabilitation: Intensive rehabilitation can help many people overcome disabilities after a stroke (see Rehabilitation: Brain Injuries). The exercises and training of rehabilitation encourage unaffected areas of the brain to learn to perform functions that were done by the damaged area. Also, people are taught new ways to use muscles unaffected by the stroke to compensate for losses in function.
The goals of rehabilitation are the following:
1. To regain as much normal function as possible
2. To maintain and improve physical condition
3. To help people relearn old skills and learn new ones as needed
Success depends on the area of the brain damaged and the person's general physical condition, functional and cognitive abilities before the stroke, social situation, learning ability, and attitude. Patience and perseverance are crucial. Participating actively in the rehabilitation program can help people avoid or lessen depression.
Rehabilitation is started in the hospital as soon as people are physically able—usually within 1 or 2 days of admission. After discharge from the hospital, rehabilitation can be continued on an outpatient basis, in a nursing home, in a rehabilitation center, or at home. Occupational and physical therapists can suggest ways to make life easier and the home safer for people with disabilities.
Family members and friends can contribute to a person's rehabilitation by keeping in mind what effects a stroke can have, so that they can better understand and support the person. Support groups can provide emotional encouragement and practical advice for people who have had a stroke and for those who care for them.
End-of-Life Issues
For some people who have had a stroke, quality of life is predicted to remain very poor despite treatment. For such people, care focuses on control of pain, comfort measures, and provision of fluids and nourishment. People who have had a stroke should establish advance directives (seeLegal and Ethical Issues: Advance Directives) as soon as possible because the recurrence and progression of strokes are unpredictable. Advance directives can help a doctor determine what kind of medical care people want if they become unable to make these decisions.
Notes and Comments
Stroke
Stroke
Classification and external resources
CT scan slice of the brain showing a right-hemispheric ischemic stroke (left side of image).
ICD-10 I61.-I64.
ICD-9 434.91
OMIM 601367
DiseasesDB 2247
MedlinePlus 000726
eMedicine neuro/9 emerg/558 emerg/557 pmr/187
MeSH D020521
A stroke, known medically as a cerebrovascular accident (CVA), is the rapidly developing loss of brain function(s) due to disturbance in the blood supply to the brain. This can be due to ischemia (lack of blood flow) caused by blockage (thrombosis, arterial embolism), or a hemorrhage (leakage of blood).[1] As a result, the affected area of the brain is unable to function, leading to inability to move one or more limbs on one side of the body, inability to understand or formulate speech, or an inability to see one side of the visual field.[2]
A stroke is a medical emergency and can cause permanent neurological damage, complications, and even death. It is the leading cause of adult disability in the United States and Europe and it is the number two cause of death worldwide.[3] Risk factors for stroke include advanced age, hypertension (high blood pressure), previous stroke or transient ischemic attack (TIA), diabetes, high cholesterol, cigarette smoking and atrial fibrillation.[4] High blood pressure is the most important modifiable risk factor of stroke.[2]
A stroke is occasionally treated in a hospital with thrombolysis (also known as a "clot buster"). Post-stroke prevention may involve the administration of antiplatelet drugs such as aspirin and dipyridamole, control and reduction of hypertension, the use of statins, and in selected patients with carotid endarterectomy, the use of anticoagulants.[2] Treatment to recover any lost function is stroke rehabilitation, involving health professions such as speech and language therapy, physical therapy and occupational therapy.
Contents [hide]
1 Definition
2 Classification
2.1 Ischemic stroke
2.2 Hemorrhagic stroke
3 Signs and symptoms
3.1 Early recognition
3.2 Subtypes
3.3 Associated symptoms
4 Causes
5 Pathophysiology
5.1 Ischemic
5.2 Hemorrhagic
6 Diagnosis
6.1 Physical examination
6.2 Imaging
6.3 Underlying etiology
7 Prevention
7.1 Risk factors
7.1.1 Blood pressure
7.1.2 Atrial fibrillation
7.1.3 Blood lipids
7.1.4 Diabetes mellitus
7.1.5 Anticoagulation drugs
7.1.6 Surgery
7.1.7 Nutritional and metabolic interventions
8 Treatment
8.1 Stroke unit
8.2 Treatment of ischemic stroke
8.2.1 Thrombolysis
8.2.2 Mechanical thrombectomy
8.2.3 Angioplasty and stenting
8.2.4 Therapeutic hypothermia
8.3 Secondary prevention of ischemic stroke
8.4 Treatment of hemorrhagic stroke
8.5 Care and rehabilitation
9 Prognosis
10 Epidemiology
11 History
12 References
13 Further reading
[edit]Definition
The traditional definition of stroke, devised by the World Health Organization in the 1970s,[5] is a "neurological deficit of cerebrovascular cause that persists beyond 24 hours or is interrupted by death within 24 hours". This definition was supposed to reflect the reversibility of tissue damage and was devised for the purpose, with the time frame of 24 hours being chosen arbitrarily. The 24-hour limit divides stroke from transient ischemic attack, which is a related syndrome of stroke symptoms that resolve completely within 24 hours.[2] With the availability of treatments that, when given early, can reduce stroke severity, many now prefer alternative concepts, such as brain attack and acute ischemic cerebrovascular syndrome (modeled after heart attack and acute coronary syndrome respectively), that reflect the urgency of stroke symptoms and the need to act swiftly.[6]
[edit]Classification
A slice of brain from the autopsy of a person who suffered an acute middle cerebral artery (MCA) stroke
Strokes can be classified into two major categories: ischemic and hemorrhagic.[7] Ischemic strokes are those that are caused by interruption of the blood supply, while hemorrhagic strokes are the ones which result from rupture of a blood vessel or an abnormal vascular structure. About 87% of strokes are caused by ischemia, and the remainder by hemorrhage. Some hemorrhages develop inside areas of ischemia ("hemorrhagic transformation"). It is unknown how many hemorrhages actually start as ischemic stroke.[2]
[edit]Ischemic stroke
Main articles: Cerebral infarction and Brain ischemia
In an ischemic stroke, blood supply to part of the brain is decreased, leading to dysfunction of the brain tissue in that area. There are four reasons why this might happen:
Thrombosis (obstruction of a blood vessel by a blood clot forming locally)
Embolism (obstruction due to an embolus from elsewhere in the body, see below),[2]
Systemic hypoperfusion (general decrease in blood supply, e.g. in shock)[8]
Venous thrombosis.[9]
Stroke without an obvious explanation is termed "cryptogenic" (of unknown origin); this constitutes 30-40% of all ischemic strokes.[2][10]
There are various classification systems for acute ischemic stroke. The Oxford Community Stroke Project classification (OCSP, also known as the Bamford or Oxford classification) relies primarily on the initial symptoms; based on the extent of the symptoms, the stroke episode is classified as total anterior circulation infarct (TACI), partial anterior circulation infarct (PACI), lacunar infarct (LACI) or posterior circulation infarct (POCI). These four entities predict the extent of the stroke, the area of the brain affected, the underlying cause, and the prognosis.[11][12] The TOAST (Trial of Org 10172 in Acute Stroke Treatment) classification is based on clinical symptoms as well as results of further investigations; on this basis, a stroke is classified as being due to (1) thrombosis or embolism due to atherosclerosis of a large artery, (2) embolism of cardiac origin, (3) occlusion of a small blood vessel, (4) other determined cause, (5) undetermined cause (two possible causes, no cause identified, or incomplete investigation).[2][13]
[edit]Hemorrhagic stroke
Main articles: Intracranial hemorrhage and intracerebral hemorrhage
CT scan showing an intracerebral hemorrhage with associated intraventricular hemorrhage.
Intracranial hemorrhage is the accumulation of blood anywhere within the skull vault. A distinction is made between intra-axial hemorrhage (blood inside the brain) and extra-axial hemorrhage (blood inside the skull but outside the brain). Intra-axial hemorrhage is due to intraparenchymal hemorrhage or intraventricular hemorrhage (blood in the ventricular system). The main types of extra-axial hemorrhage are epidural hematoma (bleeding between the dura mater and the skull), subdural hematoma (in the subdural space) and subarachnoid hemorrhage (between the arachnoid mater and pia mater). Most of the hemorrhagic stroke syndromes have specific symptoms (e.g. headache, previous head injury).
[edit]Signs and symptoms
Stroke symptoms typically start suddenly, over seconds to minutes, and in most cases do not progress further. The symptoms depend on the area of the brain affected. The more extensive the area of brain affected, the more functions that are likely to be lost. Some forms of stroke can cause additional symptoms. For example, in intracranial hemorrhage, the affected area may compress other structures. Most forms of stroke are not associated with headache, apart from subarachnoid hemorrhage and cerebral venous thrombosis and occasionally intracerebral hemorrhage.
[edit]Early recognition
Various systems have been proposed to increase recognition of stroke by patients, relatives and emergency first responders. A systematic review, updating a previous systematic review from 1994, looked at a number of trials to evaluate how well different physical examination findings are able to predict the presence or absence of stroke. It was found that sudden-onset face weakness, arm drift (e.g. if a person, when asked to raise both arms, involuntarily lets one arm drift downward) and abnormal speech are the findings most likely to lead to the correct identification of a case of stroke (+ likelihood ratio of 5.5 when at least one of these is present). Similarly, when all three of these are absent, the likelihood of stroke is significantly decreased (– likelihood ratio of 0.39).[14] While these findings are not perfect for diagnosing stroke, the fact that they can be evaluated relatively rapidly and easily make them very valuable in the acute setting.
Proposed systems include FAST (face, arm, speech, and time),[15] as advocated by the Department of Health (United Kingdom) and The Stroke Association, the American Stroke Association (www.strokeassociation.org) , National Stroke Association (US www.stroke.org), the Los Angeles Prehospital Stroke Screen (LAPSS)[16] and the Cincinnati Prehospital Stroke Scale (CPSS).[17] Use of these scales is recommended by professional guidelines.[18]
For people referred to the emergency room, early recognition of stroke is deemed important as this can expedite diagnostic tests and treatments. A scoring system called ROSIER (recognition of stroke in the emergency room) is recommended for this purpose; it is based on features from the medical history and physical examination.[18][19]
[edit]Subtypes
If the area of the brain affected contains one of the three prominent central nervous system pathways—the spinothalamic tract, corticospinal tract, and dorsal column (medial lemniscus), symptoms may include:
hemiplegia and muscle weakness of the face
numbness
reduction in sensory or vibratory sensation
In most cases, the symptoms affect only one side of the body (unilateral). Depending on the part of the brain affected, the defect in the brain is usually on the opposite side of the body. However, since these pathways also travel in the spinal cord and any lesion there can also produce these symptoms, the presence of any one of these symptoms does not necessarily indicate a stroke.
In addition to the above CNS pathways, the brainstem also consists of the 12 cranial nerves. A stroke affecting the brain stem therefore can produce symptoms relating to deficits in these cranial nerves:
altered smell, taste, hearing, or vision (total or partial)
drooping of eyelid (ptosis) and weakness of ocular muscles
decreased reflexes: gag, swallow, pupil reactivity to light
decreased sensation and muscle weakness of the face
balance problems and nystagmus
altered breathing and heart rate
weakness in sternocleidomastoid muscle with inability to turn head to one side
weakness in tongue (inability to protrude and/or move from side to side)
If the cerebral cortex is involved, the CNS pathways can again be affected, but also can produce the following symptoms:
aphasia (inability to speak or understand language from involvement of Broca's or Wernicke's area)
apraxia (altered voluntary movements)
visual field defect
memory deficits (involvement of temporal lobe)
hemineglect (involvement of parietal lobe)
disorganized thinking, confusion, hypersexual gestures (with involvement of frontal lobe)
anosognosia (persistent denial of the existence of a, usually stroke-related, deficit)
If the cerebellum is involved, the patient may have the following:
trouble walking
altered movement coordination
vertigo and or disequilibrium
[edit]Associated symptoms
Loss of consciousness, headache, and vomiting usually occurs more often in hemorrhagic stroke than in thrombosis because of the increased intracranial pressure from the leaking blood compressing on the brain.
If symptoms are maximal at onset, the cause is more likely to be a subarachnoid hemorrhage or an embolic stroke.
[edit]Causes
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Thrombotic stroke
In thrombotic stroke a thrombus (blood clot) usually forms around atherosclerotic plaques. Since blockage of the artery is gradual, onset of symptomatic thrombotic strokes is slower. A thrombus itself (even if non-occluding) can lead to an embolic stroke (see below) if the thrombus breaks off, at which point it is called an "embolus." Two types of thrombosis can cause stroke:
Large vessel disease involves the common and internal carotids, vertebral, and the Circle of Willis. Diseases that may form thrombi in the large vessels include (in descending incidence): atherosclerosis, vasoconstriction (tightening of the artery), aortic, carotid or vertebral artery dissection, various inflammatory diseases of the blood vessel wall (Takayasu arteritis, giant cell arteritis, vasculitis), noninflammatory vasculopathy, Moyamoya disease and fibromuscular dysplasia.
Small vessel disease involves the smaller arteries inside the brain: branches of the circle of Willis, middle cerebral artery, stem, and arteries arising from the distal vertebral and basilar artery. Diseases that may form thrombi in the small vessels include (in descending incidence): lipohyalinosis (build-up of fatty hyaline matter in the blood vessel as a result of high blood pressure and aging) and fibrinoid degeneration (stroke involving these vessels are known as lacunar infarcts) and microatheroma (small atherosclerotic plaques).
Sickle cell anemia, which can cause blood cells to clump up and block blood vessels, can also lead to stroke. A stroke is the second leading killer of people under 20 who suffer from sickle-cell anemia.[20]
Embolic stroke
An embolic stroke refers to the blockage of an artery by an arterial embolus, a travelling particle or debris in the arterial bloodstream originating from elsewhere. An embolus is most frequently a thrombus, but it can also be a number of other substances including fat (e.g. from bone marrow in a broken bone), air, cancer cells or clumps of bacteria (usually from infectious endocarditis).
Because an embolus arises from elsewhere, local therapy only solves the problem temporarily. Thus, the source of the embolus must be identified. Because the embolic blockage is sudden in onset, symptoms usually are maximal at start. Also, symptoms may be transient as the embolus is partially resorbed and moves to a different location or dissipates altogether.
Emboli most commonly arise from the heart (especially in atrial fibrillation) but may originate from elsewhere in the arterial tree. In paradoxical embolism, a deep vein thrombosis embolises through an atrial or ventricular septal defect in the heart into the brain.
Cardiac causes can be distinguished between high and low-risk:[21]
High risk: atrial fibrillation and paroxysmal atrial fibrillation, rheumatic disease of the mitral or aortic valve disease, artificial heart valves, known cardiac thrombus of the atrium or vertricle, sick sinus syndrome, sustained atrial flutter, recent myocardial infarction, chronic myocardial infarction together with ejection fraction <28 percent, symptomatic congestive heart failure with ejection fraction <30 percent, dilated cardiomyopathy, Libman-Sacks endocarditis, Marantic endocarditis, infective endocarditis, papillary fibroelastoma, left atrial myxoma and coronary artery bypass graft (CABG) surgery
Low risk/potential: calcification of the annulus (ring) of the mitral valve, patent foramen ovale (PFO), atrial septal aneurysm, atrial septal aneurysm with patent foramen ovale, left ventricular aneurysm without thrombus, isolated left atrial "smoke" on echocardiography (no mitral stenosis or atrial fibrillation), complex atheroma in the ascending aorta or proximal arch
Systemic hypoperfusion
Systemic hypoperfusion is the reduction of blood flow to all parts of the body. It is most commonly due to cardiac pump failure from cardiac arrest or arrhythmias, or from reduced cardiac output as a result of myocardial infarction, pulmonary embolism, pericardial effusion, or bleeding. Hypoxemia (low blood oxygen content) may precipitate the hypoperfusion. Because the reduction in blood flow is global, all parts of the brain may be affected, especially "watershed" areas - border zone regions supplied by the major cerebral arteries. A watershed stroke refers to the condition when blood supply to these areas is compromised. Blood flow to these areas does not necessarily stop, but instead it may lessen to the point where brain damage can occur. This phenomenon is also referred to as "last meadow" to point to the fact that in irrigation the last meadow receives the least amount of water.
Venous thrombosis
Cerebral venous sinus thrombosis leads to stroke due to locally increased venous pressure, which exceeds the pressure generated by the arteries. Infarcts are more likely to undergo hemorrhagic transformation (leaking of blood into the damaged area) than other types of ischemic stroke.[9]
Intracerebral hemorrhage
It generally occurs in small arteries or arterioles and is commonly due to hypertension, intracranial vascular malformations (including cavernous angiomas or arteriovenous malformations), cerebral amyloid angiopathy, or infarcts into which secondary haemorrhage has occurred.[2] Other potential causes are trauma, bleeding disorders, amyloid angiopathy, illicit drug use (e.g. amphetamines or cocaine). The hematoma enlarges until pressure from surrounding tissue limits its growth, or until it decompresses by emptying into the ventricular system, CSF or the pial surface. A third of intracerebral bleed is into the brain's ventricles. ICH has a mortality rate of 44 percent after 30 days, higher than ischemic stroke or even the very deadly subarachnoid hemorrhage (which, however, also may be classified as a type of stroke[2]).
[edit]Pathophysiology
[edit]Ischemic
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Ischemic stroke occurs due to a loss of blood supply to part of the brain, initiating the ischemic cascade.[22] Brain tissue ceases to function if deprived of oxygen for more than 60 to 90 seconds and after approximately three hours, will suffer irreversible injury possibly leading to death of the tissue, i.e., infarction. (This is why TPA's (e.g. Streptokinase, Altapase) are given only until three hours since the onset of the stroke.) Atherosclerosis may disrupt the blood supply by narrowing the lumen of blood vessels leading to a reduction of blood flow, by causing the formation of blood clots within the vessel, or by releasing showers of small emboli through the disintegration of atherosclerotic plaques. Embolic infarction occurs when emboli formed elsewhere in the circulatory system, typically in the heart as a consequence of atrial fibrillation, or in the carotid arteries, break off, enter the cerebral circulation, then lodge in and occlude brain blood vessels. Since blood vessels in the brain are now occluded, the brain becomes low in energy, and thus it resorts into using anaerobic respiration within the region of brain tissue affected by ischemia. Unfortunately, this kind of respiration produces less ATP but releases a by-product called lactic acid. Lactic acid is an irritant which could potentially destroy cells since it is an acid and disrupts the normal acid-bace balance in the brain. The ischemia area is referred to as the "ischemic penumbra".[23]
Then, as oxygen or glucose becomes depleted in ischemic brain tissue, the production of high energy phosphate compounds such as adenosine triphosphate (ATP) fails, leading to failure of energy-dependent processes (such as ion pumping) necessary for tissue cell survival. This sets off a series of interrelated events that result in cellular injury and death. A major cause of neuronal injury is release of the excitatory neurotransmitter glutamate. The concentration of glutamate outside the cells of the nervous system is normally kept low by so-called uptake carriers, which are powered by the concentration gradients of ions (mainly Na+) across the cell membrane. However, stroke cuts off the supply of oxygen and glucose which powers the ion pumps maintaining these gradients. As a result the transmembrane ion gradients run down, and glutamate transporters reverse their direction, releasing glutamate into the extracellular space. Glutamate acts on receptors in nerve cells (especially NMDA receptors), producing an influx of calcium which activates enzymes that digest the cells' proteins, lipids and nuclear material. Calcium influx can also lead to the failure of mitochondria, which can lead further toward energy depletion and may trigger cell death due to apoptosis.
Ischemia also induces production of oxygen free radicals and other reactive oxygen species. These react with and damage a number of cellular and extracellular elements. Damage to the blood vessel lining or endothelium is particularly important. In fact, many antioxidant neuroprotectants such as uric acid and NXY-059 work at the level of the endothelium and not in the brain per se. Free radicals also directly initiate elements of the apoptosis cascade by means of redox signaling.[20]
These processes are the same for any type of ischemic tissue and are referred to collectively as the ischemic cascade. However, brain tissue is especially vulnerable to ischemia since it has little respiratory reserve and is completely dependent on aerobic metabolism, unlike most other organs.
Brain tissue survival can be improved to some extent if one or more of these processes is inhibited. Drugs that scavenge reactive oxygen species, inhibit apoptosis, or inhibit excitatory neurotransmitters, for example, have been shown experimentally to reduce tissue injury due to ischemia. Agents that work in this way are referred to as being neuroprotective. Until recently, human clinical trials with neuroprotective agents have failed, with the probable exception of deep barbiturate coma. However, more recently NXY-059, the disulfonyl derivative of the radical-scavenging spintrap phenylbutylnitrone, is reported to be neuroprotective in stroke.[24] This agent appears to work at the level of the blood vessel lining or endothelium. Unfortunately, after producing favorable results in one large-scale clinical trial, a second trial failed to show favorable results.[20]
In addition to injurious effects on brain cells, ischemia and infarction can result in loss of structural integrity of brain tissue and blood vessels, partly through the release of matrix metalloproteases, which are zinc- and calcium-dependent enzymes that break down collagen, hyaluronic acid, and other elements of connective tissue. Other proteases also contribute to this process. The loss of vascular structural integrity results in a breakdown of the protective blood brain barrier that contributes to cerebral edema, which can cause secondary progression of the brain injury.
As is the case with any type of brain injury, the immune system is activated by cerebral infarction and may under some circumstances exacerbate the injury caused by the infarction. Inhibition of the inflammatory response has been shown experimentally to reduce tissue injury due to cerebral infarction, but this has not proved out in clinical studies.
[edit]Hemorrhagic
Head CT showing deep intracerebral hemorrhage due to bleeding within the cerebellum, approximately 30 hours old.
Hemorrhagic strokes result in tissue injury by causing compression of tissue from an expanding hematoma or hematomas. This can distort and injure tissue. In addition, the pressure may lead to a loss of blood supply to affected tissue with resulting infarction, and the blood released by brain hemorrhage appears to have direct toxic effects on brain tissue and vasculature.[20]
[edit]Diagnosis
Stroke is diagnosed through several techniques: a neurological examination (such as the Nihss), CT scans (most often without contrast enhancements) or MRI scans, Doppler ultrasound, and arteriography. The diagnosis of stroke itself is clinical, with assistance from the imaging techniques. Imaging techniques also assist in determining the subtypes and cause of stroke. There is yet no commonly used blood test for the stroke diagnosis itself, though blood tests may be of help in finding out the likely cause of stroke.[25]
[edit]Physical examination
A physical examination, including taking a medical history of the symptoms and a neurological status, helps giving an evaluation of the location and severity of a stroke. It can give a standard score on e.g. the NIH stroke scale.
[edit]Imaging
For diagnosing ischemic stroke in the emergency setting:[26]
CT scans (without contrast enhancements)
sensitivity= 16%
specificity= 96%
MRI scan
sensitivity= 83%
specificity= 98%
For diagnosing hemorrhagic stroke in the emergency setting:
CT scans (without contrast enhancements)
sensitivity= 89%
specificity= 100%
MRI scan
sensitivity= 81%
specificity= 100%
For detecting chronic hemorrhages, MRI scan is more sensitive.[27]
For the assessment of stable stroke, nuclear medicine scans SPECT and PET/CT may be helpful. SPECT documents cerebral blood flow and PET with FDG isotope the metabolic activity of the neurons.
[edit]Underlying etiology
When a stroke has been diagnosed, various other studies may be performed to determine the underlying etiology. With the current treatment and diagnosis options available, it is of particular importance to determine whether there is a peripheral source of emboli. Test selection may vary, since the cause of stroke varies with age, comorbidity and the clinical presentation. Commonly used techniques include:
an ultrasound/doppler study of the carotid arteries (to detect carotid stenosis) or dissection of the precerebral arteries
an electrocardiogram (ECG) and echocardiogram (to identify arrhythmias and resultant clots in the heart which may spread to the brain vessels through the bloodstream)
a Holter monitor study to identify intermittent arrhythmias
an angiogram of the cerebral vasculature (if a bleed is thought to have originated from an aneurysm or arteriovenous malformation)
blood tests to determine hypercholesterolemia, bleeding diathesis and some rarer causes such as homocysteinuria
[edit]Prevention
Given the disease burden of stroke, prevention is an important public health concern.[28] Primary prevention is less effective than secondary prevention (as judged by the number needed to treat to prevent one stroke per year).[28] Recent guidelines detail the evidence for primary prevention in stroke.[29] Because stroke may indicate underlying atherosclerosis, it is important to determine the patient's risk for other cardiovascular diseases such as coronary heart disease. Conversely, aspirin prevents against first stroke in patients who have suffered a myocardial infarction or patients with a high cardiovascular risk.[30][31]
[edit]Risk factors
The most important modifiable risk factors for stroke are high blood pressure and atrial fibrillation (although magnitude of this effect is small: the evidence from the Medical Research Council trials is that 833 patients have to be treated for 1 year to prevent one stroke[32][33]). Other modifiable risk factors include high blood cholesterol levels, diabetes, cigarette smoking[34][35] (active and passive), heavy alcohol consumption[36] and drug use,[37] lack of physical activity, obesity and unhealthy diet.[38] Alcohol use could predispose to ischemic stroke, and intracerebral and subarachnoid hemorrhage via multiple mechanisms (for example via hypertension, atrial fibrillation, rebound thrombocytosis and platelet aggregation and clotting disturbances).[39] The drugs most commonly associated with stroke are cocaine, amphetamines causing hemorrhagic stroke, but also over-the-counter cough and cold drugs containing sympathomimetics.[40][41]
No high quality studies have shown the effectiveness of interventions aimed at weight reduction, promotion of regular exercise, reducing alcohol consumption or smoking cessation.[42] Nonetheless, given the large body of circumstantial evidence, best medical management for stroke includes advice on diet, exercise, smoking and alcohol use.[43] Medication or drug therapy is the most common method of stroke prevention; carotid endarterectomy can be a useful surgical method of preventing stroke.
[edit]Blood pressure
Hypertension accounts for 35-50% of stroke risk.[44] Epidemiological studies suggest that even a small blood pressure reduction (5 to 6 mmHg systolic, 2 to 3 mmHg diastolic) would result in 40% fewer strokes.[45] Lowering blood pressure has been conclusively shown to prevent both ischemic and hemorrhagic strokes.[46][47] It is equally important in secondary prevention.[48] Even patients older than 80 years and those with isolated systolic hypertension benefit from antihypertensive therapy.[49][50][51] Studies show that intensive antihypertensive therapy results in a greater risk reduction.[52] The available evidence does not show large differences in stroke prevention between antihypertensive drugs —therefore, other factors such as protection against other forms of cardiovascular disease should be considered and cost.[52][53]
[edit]Atrial fibrillation
Patients with atrial fibrillation have a risk of 5% each year to develop stroke, and this risk is even higher in those with valvular atrial fibrillation.[54] Depending on the stroke risk, anticoagulation with medications such as coumarins or aspirin is warranted for stroke prevention.[55]
[edit]Blood lipids
High cholesterol levels have been inconsistently associated with (ischemic) stroke.[47][56] Statins have been shown to reduce the risk of stroke by about 15%.[57] Since earlier meta-analyses of other lipid-lowering drugs did not show a decreased risk,[58] statins might exert their effect through mechanisms other than their lipid-lowering effects.[57]
[edit]Diabetes mellitus
Patients with diabetes mellitus are 2 to 3 times more likely to develop stroke, and they commonly have hypertension and hyperlipidemia. Intensive disease control has been shown to reduce microvascular complications such as nephropathy and retinopathy but not macrovascular complications such as stroke.[59][60]
[edit]Anticoagulation drugs
Oral anticoagulants such as warfarin have been the mainstay of stroke prevention for over 50 years. However, several studies have shown that aspirin and antiplatelet drugs are highly effective in secondary prevention after a stroke or transient ischemic attack[30]. Low doses of aspirin (for example 75–150 mg) are as effective as high doses but have fewer side effects; the lowest effective dose remains unknown.[61] Thienopyridines (clopidogrel, ticlopidine) "might be slightly more effective" than aspirin and have a decreased risk of gastrointestinal bleeding, but they are more expensive.[62] Their exact role remains controversial. Ticlopidine has more skin rash, diarrhea, neutropenia and thrombotic thrombocytopenic purpura.[62] Dipyridamole can be added to aspirin therapy to provide a small additional benefit, even though headache is a common side effect.[63] Low-dose aspirin is also effective for stroke prevention after sustaining a myocardial infarction.[31] Oral anticoagulants are not advised for stroke prevention —any benefit is offset by bleeding risk.[64]
In primary prevention however, antiplatelet drugs did not reduce the risk of ischemic stroke while increasing the risk of major bleeding.[65][66] Further studies are needed to investigate a possible protective effect of aspirin against ischemic stroke in women.[67][68]
[edit]Surgery
Surgical procedures such as carotid endarterectomy or carotid angioplasty can be used to remove significant atherosclerotic narrowing (stenosis) of the carotid artery, which supplies blood to the brain. There is a large body of evidence supporting this procedure in selected cases.[43] Endarterectomy for a significant stenosis has been shown to be useful in the secondary prevention after a previous symptomatic stroke.[69] Carotid artery stenting has not been shown to be equally useful.[70][71] Patients are selected for surgery based on age, gender, degree of stenosis, time since symptoms and patients' preferences.[43] Surgery is most efficient when not delayed too long —the risk of recurrent stroke in a patient who has a 50% or greater stenosis is up to 20% after 5 years, but endarterectomy reduces this risk to around 5%. The number of procedures needed to cure one patient was 5 for early surgery (within two weeks after the initial stroke), but 125 if delayed longer than 12 weeks.[72][73]
Screening for carotid artery narrowing has not been shown to be a useful screening test in the general population.[74] Studies of surgical intervention for carotid artery stenosis without symptoms have shown only a small decrease in the risk of stroke.[75][76] To be beneficial, the complication rate of the surgery should be kept below 4%. Even then, for 100 surgeries, 5 patients will benefit by avoiding stroke, 3 will develop stroke despite surgery, 3 will develop stroke or die due to the surgery itself, and 89 will remain stroke-free but would also have done so without intervention.[43]
[edit]Nutritional and metabolic interventions
Nutrition, specifically the Mediterranean-style diet, has the potential of more than halving stroke risk.[77]
With regards to lowering homocysteine, a meta-analysis of previous trials has concluded that lowering homocysteine with folic acid and other supplements may reduce stroke risk.[78] However, the two largest randomized controlled trials included in the meta-analysis had conflicting results. One reported positve results;[79] whereas the other was negative.[80]
The European Society of Cardiology and the European Association for Cardiovascular Prevention and Rehabilitation have developed an interactive tool for prediction and managing the risk of heart attack and stroke in Europe. HeartScore is aimed at supporting clinicians in optimising individual cardiovascular risk reduction. The Heartscore Programme is available in 12 languages and offers web based or PC version [81].
[edit]Treatment
[edit]Stroke unit
Ideally, people who have had a stroke are admitted to a "stroke unit", a ward or dedicated area in hospital staffed by nurses and therapists with experience in stroke treatment. It has been shown that people admitted to a stroke unit have a higher chance of surviving than those admitted elsewhere in hospital, even if they are being cared for by doctors without experience in stroke.[2]
When an acute stroke is suspected by history and physical examination, the goal of early assessment is to determine the cause. Treatment varies according to the underlying cause of the stroke, thromboembolic (ischemic) or hemorrhagic. A non-contrast head CT scan can rapidly identify a hemorrhagic stroke by imaging bleeding in or around the brain. If no bleeding is seen, a presumptive diagnosis of ischemic stroke is made.
[edit]Treatment of ischemic stroke
An ischemic stroke is caused by a thrombus (blood clot) occluding blood flow to an artery supplying the brain. Definitive therapy is aimed at removing the blockage by breaking the clot down (thrombolysis), or by removing it mechanically (thrombectomy). The more rapidly blood flow is restored to the brain, the fewer brain cells die.[82]
Other medical therapies are aimed at minimizing clot enlargement or preventing new clots from forming. To this end, treatment with medications such as aspirin, clopidogrel and dipyridamole may be given to prevent platelets from aggregating[30].
In addition to definitive therapies, management of acute stroke includes control of blood sugars, ensuring the patient has adequate oxygenation and adequate intravenous fluids. Patients may be positioned with their heads flat on the stretcher, rather than sitting up, to increase blood flow to the brain. It is common for the blood pressure to be elevated immediately following a stroke. Although high blood pressure may cause some strokes, hypertension during acute stroke is desirable to allow adequate blood flow to the brain.
[edit]Thrombolysis
In increasing numbers of primary stroke centers, pharmacologic thrombolysis ("clot busting") with the drug tissue plasminogen activator (tPA), is used to dissolve the clot and unblock the artery. However, the use of tPA in acute stroke is controversial. On one hand, it is endorsed by the American Heart Association and the American Academy of Neurology as the recommended treatment for acute stroke within three hours of onset of symptoms as long as there are not other contraindications (such as abnormal lab values, high blood pressure, or recent surgery). This position for tPA is based upon the findings of two studies by one group of investigators[83] which showed that tPA improves the chances for a good neurological outcome. When administered within the first three hours, 39% of all patients who were treated with tPA had a good outcome at three months, only 26% of placebo controlled patients had a good functional outcome.
A recent study using alteplase for thrombolysis in ischemic stroke suggests clinical benefit with administration 3 to 4.5 hours after stroke onset.[84] However, in the NINDS trial 6.4% of patients with large strokes developed substantial brain hemorrhage as a complication from being given tPA. A recent study found the mortality to be higher among patients receiving tPA versus those who did not.[85] Additionally, it is the position of the American Academy of Emergency Medicine that objective evidence regarding the efficacy, safety, and applicability of tPA for acute ischemic stroke is insufficient to warrant its classification as standard of care.[86].
Intra-artial fibrinolysis, where a catherter is passed up an artery into the brain and the medication is injected at the site of thrombosis, has been found to improve outcomes in people with acute ischemic stroke.[87][original research?]
[edit]Mechanical thrombectomy
Merci Retriever L5.
Another intervention for acute ischemic stroke is removal of the offending thrombus directly. This is accomplished by inserting a catheter into the femoral artery, directing it into the cerebral circulation, and deploying a corkscrew-like device to ensnare the clot, which is then withdrawn from the body. Mechanical embolectomy devices have been demonstrated effective at restoring blood flow in patients who were unable to receive thrombolytic drugs or for whom the drugs were ineffective,[88][89][90][91] though no differences have been found between newer and older versions of the devices.[92] The devices have only been tested on patients treated with mechanical clot embolectomy within eight hours of the onset of symptoms.
[edit]Angioplasty and stenting
Angioplasty and stenting have begun to be looked at as possible viable options in treatment of acute ischemic stroke. In a systematic review of six uncontrolled, single-center trials, involving a total of 300 patients, of intra-cranial stenting in symptomatic intracranial arterial stenosis, the rate of technical success (reduction to stenosis of <50%) ranged from 90-98%, and the rate of major peri-procedural complications ranged from 4-10%. The rates of restenosis and/or stroke following the treatment were also favorable.[93] This data suggests that a large, randomized controlled trial is needed to more completely evaluate the possible therapeutic advantage of this treatment.
[edit]Therapeutic hypothermia
Main article: therapeutic hypothermia
Most of the data concerning therapeutic hypothermia’s effectiveness in treating ischemic stroke is limited to animal studies. These studies have focused primarily on ischemic as opposed to hemorrhagic stroke, as hypothermia has been associated with a lower clotting threshold. In these animal studies investigating the effect of temperature decline following ischemic stroke, hypothermia has been shown to be an effective all-purpose neuroprotectant.[94] This promising data has led to the initiation of a variety of human studies. At the time of this article’s publishing, this research has yet to return results. However, in terms of feasibility, the use of hypothermia to control intracranial pressure (ICP) after an ischemic stroke was found to be both safe and practical. The device used in this study was called the Arctic Sun.[95]
[edit]Secondary prevention of ischemic stroke
Anticoagulation can prevent recurrent stroke. Among patients with nonvalvular atrial fibrillation, anticoagulation can reduce stroke by 60% while antiplatelet agents can reduce stroke by 20%.[96]. However, a recent meta-analysis suggests harm from anti-coagulation started early after an embolic stroke.[97] Stroke prevention treatment for atrial fibrillation is determined according to the CHADS/CHADS2 system.
If studies show carotid stenosis, and the patient has residual function in the affected side, carotid endarterectomy (surgical removal of the stenosis) may decrease the risk of recurrence if performed rapidly after stroke.
[edit]Treatment of hemorrhagic stroke
Patients with intracerebral hemorrhage require neurosurgical evaluation to detect and treat the cause of the bleeding, although many may not need surgery. Anticoagulants and antithrombotics, key in treating ischemic stroke, can make bleeding worse and cannot be used in intracerebral hemorrhage. Patients are monitored and their blood pressure, blood sugar, and oxygenation are kept at optimum levels.
[edit]Care and rehabilitation
Stroke rehabilitation is the process by which patients with disabling strokes undergo treatment to help them return to normal life as much as possible by regaining and relearning the skills of everyday living. It also aims to help the survivor understand and adapt to difficulties, prevent secondary complications and educate family members to play a supporting role.
A rehabilitation team is usually multidisciplinary as it involves staff with different skills working together to help the patient. These include nursing staff, physiotherapy, occupational therapy, speech and language therapy, and usually a physician trained in rehabilitation medicine. Some teams may also include psychologists, social workers, and pharmacists since at least one third of the patients manifest post stroke depression. Validated instruments such as the Barthel scale may be used to assess the likelihood of a stroke patient being able to manage at home with or without support subsequent to discharge from hospital.
Good nursing care is fundamental in maintaining skin care, feeding, hydration, positioning, and monitoring vital signs such as temperature, pulse, and blood pressure. Stroke rehabilitation begins almost immediately.
For most stroke patients, physical therapy (PT) and occupational therapy (OT) are the cornerstones of the rehabilitation process, but in many countries Neurocognitive Rehabilitation is used, too. Often, assistive technology such as a wheelchair, walkers, canes, and orthosis may be beneficial. PT and OT have overlapping areas of working but their main attention fields are; PT involves re-learning functions as transferring, walking and other gross motor functions. OT focusses on exercises and training to help relearn everyday activities known as the Activities of daily living (ADLs) such as eating, drinking, dressing, bathing, cooking, reading and writing, and toileting. Speech and language therapy is appropriate for patients with problems understanding speech or written words, problems forming speech and problems with swallowing.
Patients may have particular problems, such as complete or partial inability to swallow, which can cause swallowed material to pass into the lungs and cause aspiration pneumonia. The condition may improve with time, but in the interim, a nasogastric tube may be inserted, enabling liquid food to be given directly into the stomach. If swallowing is still unsafe after a week, then a percutaneous endoscopic gastrostomy (PEG) tube is passed and this can remain indefinitely.
Stroke rehabilitation should be started as quickly as possible and can last anywhere from a few days to over a year. Most return of function is seen in the first few months, and then improvement falls off with the "window" considered officially by U.S. state rehabilitation units and others to be closed after six months, with little chance of further improvement. However, patients have been known to continue to improve for years, regaining and strengthening abilities like writing, walking, running, and talking. Daily rehabilitation exercises should continue to be part of the stroke patient's routine. Complete recovery is unusual but not impossible and most patients will improve to some extent : proper diet and exercise are known to help the brain to recover.
[edit]Prognosis
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Disability affects 75% of stroke survivors enough to decrease their employability.[98] Stroke can affect patients physically, mentally, emotionally, or a combination of the three. The results of stroke vary widely depending on size and location of the lesion.[99] Dysfunctions correspond to areas in the brain that have been damaged.
Some of the physical disabilities that can result from stroke include muscle weakness, numbness, pressure sores, pneumonia, incontinence, apraxia (inability to perform learned movements), difficulties carrying out daily activities, appetite loss, speech loss, vision loss, and pain. If the stroke is severe enough, or in a certain location such as parts of the brainstem, coma or death can result.
Emotional problems resulting from stroke can result from direct damage to emotional centers in the brain or from frustration and difficulty adapting to new limitations. Post-stroke emotional difficulties include anxiety, panic attacks, flat affect (failure to express emotions), mania, apathy, and psychosis.
30 to 50% of stroke survivors suffer post stroke depression, which is characterized by lethargy, irritability, sleep disturbances, lowered self esteem, and withdrawal.[100] Depression can reduce motivation and worsen outcome, but can be treated with antidepressants.
Emotional lability, another consequence of stroke, causes the patient to switch quickly between emotional highs and lows and to express emotions inappropriately, for instance with an excess of laughing or crying with little or no provocation. While these expressions of emotion usually correspond to the patient's actual emotions, a more severe form of emotional lability causes patients to laugh and cry pathologically, without regard to context or emotion.[98] Some patients show the opposite of what they feel, for example crying when they are happy.[101] Emotional lability occurs in about 20% of stroke patients.
Cognitive deficits resulting from stroke include perceptual disorders, speech problems, dementia, and problems with attention and memory. A stroke sufferer may be unaware of his or her own disabilities, a condition called anosognosia. In a condition called hemispatial neglect, a patient is unable to attend to anything on the side of space opposite to the damaged hemisphere.
Up to 10% of all stroke patients develop seizures, most commonly in the week subsequent to the event; the severity of the stroke increases the likelihood of a seizure.[102][103]
[edit]Epidemiology
Stroke could soon be the most common cause of death worldwide.[104] Stroke is currently the second leading cause of death in the Western world, ranking after heart disease and before cancer,[2] and causes 10% of deaths worldwide.[105] Geographic disparities in stroke incidence have been observed, including the existence of a "stroke belt" in the southeastern United States, but causes of these disparities have not been explained.
The incidence of stroke increases exponentially from 30 years of age, and etiology varies by age.[106] Advanced age is one of the most significant stroke risk factors. 95% of strokes occur in people age 45 and older, and two-thirds of strokes occur in those over the age of 65.[100][20] A person's risk of dying if he or she does have a stroke also increases with age. However, stroke can occur at any age, including in fetuses.
Family members may have a genetic tendency for stroke or share a lifestyle that contributes to stroke. Higher levels of Von Willebrand factor are more common amongst people who have had ischemic stroke for the first time.[107] The results of this study found that the only significant genetic factor was the person's blood type. Having had a stroke in the past greatly increases one's risk of future strokes.
Men are 25% more likely to suffer strokes than women,[20] yet 60% of deaths from stroke occur in women.[101] Since women live longer, they are older on average when they have their strokes and thus more often killed (NIMH 2002).[20] Some risk factors for stroke apply only to women. Primary among these are pregnancy, childbirth, menopause and the treatment thereof (HRT).
[edit]History
Hippocrates first described the sudden paralysis that is often associated with stroke.
Episodes of stroke and familial stroke have been reported from the 2nd millenium BC onward in ancient Mesopotamia and Persia[108]. Hippocrates (460 to 370 BC) was first to describe the phenomenon of sudden paralysis that is often associated with ischemia. Apoplexy, from the Greek word meaning "struck down with violence,” first appeared in Hippocratic writings to describe this phenomenon.[109][110]
The word stroke was used as a synonym for apoplectic seizure as early as 1599,[111] and is a fairly literal translation of the Greek term.
In 1658, in his Apoplexia, Johann Jacob Wepfer (1620–1695) identified the cause of hemorrhagic stroke when he suggested that people who had died of apoplexy had bleeding in their brains.[109][20] Wepfer also identified the main arteries supplying the brain, the vertebral and carotid arteries, and identified the cause of ischemic stroke [also known as cerebral infarction] when he suggested that apoplexy might be caused by a blockage to those vessels.[20]
Rudolf Virchow first described the mechanism of thromboembolism as a major factor.[112]
[edit]References
^ Sims NR, Muyderman H (September 2009). "Mitochondria, oxidative metabolism and cell death in stroke". Biochimica et Biophysica Acta 1802 (1): 80–91. doi:10.1016/j.bbadis.2009.09.003. PMID 19751827.
^ a b c d e f g h i j k l Donnan GA, Fisher M, Macleod M, Davis SM (May 2008). "Stroke". Lancet 371 (9624): 1612–23. doi:10.1016/S0140-6736(08)60694-7. PMID 18468545.
^ Feigin VL (2005). "Stroke epidemiology in the developing world". Lancet 365 (9478): 2160–1. doi:10.1016/S0140-6736(05)66755-4. PMID 15978910.
^ Stroke Mount Sinai Hospital, New York
^ World Health Organisation (1978). Cerebrovascular Disorders (Offset Publications). Geneva: World Health Organization. ISBN 9241700432. OCLC 4757533.
^ Kidwell CS, Warach S (December 2003). "Acute ischemic cerebrovascular syndrome: diagnostic criteria". Stroke 34 (12): 2995–8. doi:10.1161/01.STR.0000098902.69855.A9. PMID 14605325.
^ "Brain Basics: Preventing Stroke". National Institute of Neurological Disorders and Stroke. Retrieved 2009-10-24.
^ Shuaib A, Hachinski VC (September 1991). "Mechanisms and management of stroke in the elderly". CMAJ 145 (5): 433–43. PMID 1878825.
^ a b Stam J (April 2005). "Thrombosis of the cerebral veins and sinuses". The New England Journal of Medicine 352 (17): 1791–8. doi:10.1056/NEJMra042354. PMID 15858188.
^ Guercini F, Acciarresi M, Agnelli G, Paciaroni M (April 2008). "Cryptogenic stroke: time to determine aetiology". Journal of Thrombosis and Haemostasis 6 (4): 549–54. doi:10.1111/j.1538-7836.2008.02903.x. PMID 18208534.
^ Bamford J, Sandercock P, Dennis M, Burn J, Warlow C (June 1991). "Classification and natural history of clinically identifiable subtypes of cerebral infarction". Lancet 337 (8756): 1521–6. doi:10.1016/0140-6736(91)93206-O. PMID 1675378. Later publications distinguish between "syndrome" and "infarct", based on evidence from imaging. "Syndrome" may be replaced by "hemorrhage" if imaging demonstrates a bleed. See Internet Stroke Center. "Oxford Stroke Scale". Retrieved 2008-11-14.
^ Bamford JM (2000). "The role of the clinical examination in the subclassification of stroke". Cerebrovascular Diseases 10 Suppl 4: 2–4. doi:10.1159/000047582. PMID 11070389.
^ Adams HP, Bendixen BH, Kappelle LJ, et al. (January 1993). "Classification of subtype of acute ischemic stroke. Definitions for use in a multicenter clinical trial. TOAST. Trial of Org 10172 in Acute Stroke Treatment". Stroke 24 (1): 35–41. PMID 7678184.
^ Goldstein LB, Simel DL (May 2005). "Is this patient having a stroke?". JAMA 293 (19): 2391–402. doi:10.1001/jama.293.19.2391. PMID 15900010.
^ Harbison J, Massey A, Barnett L, Hodge D, Ford GA (June 1999). "Rapid ambulance protocol for acute stroke". Lancet 353 (9168): 1935. doi:10.1016/S0140-6736(99)00966-6. PMID 10371574.
^ Kidwell CS, Saver JL, Schubert GB, Eckstein M, Starkman S (1998). "Design and retrospective analysis of the Los Angeles Prehospital Stroke Screen (LAPSS)". Prehospital Emergency Care 2 (4): 267–73. doi:10.1080/10903129808958878. PMID 9799012.
^ Kothari RU, Pancioli A, Liu T, Brott T, Broderick J (April 1999). "Cincinnati Prehospital Stroke Scale: reproducibility and validity". Annals of Emergency Medicine 33 (4): 373–8. doi:10.1016/S0196-0644(99)70299-4. PMID 10092713.
^ a b National Institute for Health and Clinical Excellence. Clinical guideline 68: Stroke. London, 2008.
^ Nor AM, Davis J, Sen B, et al. (November 2005). "The Recognition of Stroke in the Emergency Room (ROSIER) scale: development and validation of a stroke recognition instrument". Lancet Neurology 4 (11): 727–34. doi:10.1016/S1474-4422(05)70201-5. PMID 16239179.
^ a b c d e f g h i National Institute of Neurological Disorders and Stroke (NINDS) (1999). "Stroke: Hope Through Research". National Institutes of Health.
^ Ay H, Furie KL, Singhal A, Smith WS, Sorensen AG, Koroshetz WJ (November 2005). "An evidence-based causative classification system for acute ischemic stroke". Annals of Neurology 58 (5): 688–97. doi:10.1002/ana.20617. PMID 16240340.
^ Deb P, Sharma S, Hassan KM. "Pathophysiologic mechanisms of acute ischemic stroke: An overview with emphasis on therapeutic significance beyond thrombolysis". Pathophysiology. January 12, 2010. PMID 20074922.
^ Brunner and Suddarth's Textbook on Medical-Surgical Nursing, 11th Edition
^ Lees KR, Zivin JA, Ashwood T, et al. (February 2006). "NXY-059 for acute ischemic stroke". The New England Journal of Medicine 354 (6): 588–600. doi:10.1056/NEJMoa052980. PMID 16467546.
^ Hill MD (November 2005). "Diagnostic biomarkers for stroke: a stroke neurologist's perspective". Clinical Chemistry 51 (11): 2001–2. doi:10.1373/clinchem.2005.056382. PMID 16244286.
^ Chalela JA, Kidwell CS, Nentwich LM, et al. (January 2007). "Magnetic resonance imaging and computed tomography in emergency assessment of patients with suspected acute stroke: a prospective comparison". Lancet 369 (9558): 293–8. doi:10.1016/S0140-6736(07)60151-2. PMID 17258669.
^ Kidwell CS, Chalela JA, Saver JL, et al. (October 2004). "Comparison of MRI and CT for detection of acute intracerebral hemorrhage". JAMA 292 (15): 1823–30. doi:10.1001/jama.292.15.1823. PMID 15494579.
^ a b Straus SE, Majumdar SR, McAlister FA (September 2002). "New evidence for stroke prevention: scientific review". JAMA 288 (11): 1388–95. doi:10.1001/jama.288.11.1388. PMID 12234233.
^ Goldstein LB, Adams R, Alberts MJ, et al. (June 2006). "Primary prevention of ischemic stroke: a guideline from the American Heart Association/American Stroke Association Stroke Council: cosponsored by the Atherosclerotic Peripheral Vascular Disease Interdisciplinary Working Group; Cardiovascular Nursing Council; Clinical Cardiology Council; Nutrition, Physical Activity, and Metabolism Council; and the Quality of Care and Outcomes Research Interdisciplinary Working Group: the American Academy of Neurology affirms the value of this guideline". Stroke 37 (6): 1583–633. doi:10.1161/01.STR.0000223048.70103.F1. PMID 16675728.
^ a b c NPS Prescribing Practice Review 44: Antiplatelets and anticoagulants in stroke prevention (2009). Available at http://www.nps.org.au/health_professionals/publications/prescribing_practice_review/current/nps_prescribing_practice_review_44
^ a b Antithrombotic Trialists' Collaboration (January 2002). "Collaborative meta-analysis of randomised trials of antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high risk patients". BMJ 324 (7329): 71–86. doi:10.1136/bmj.324.7329.71. PMID 11786451.
^ "MRC trial of treatment of mild hypertension: principal results. Medical Research Council Working Party". British Medical Journal 291 (6488): 97–104. July 1985. doi:10.1136/bmj.291.6488.97. PMID 2861880.
^ Thomson R (2009). "Evidence based implementation of complex interventions". BMJ 339: b3124. doi:10.1136/bmj.b3124. PMID 19675081.
^ Hankey GJ (August 1999). "Smoking and risk of stroke". Journal of Cardiovascular Risk 6 (4): 207–11. PMID 10501270.
^ Wannamethee SG, Shaper AG, Whincup PH, Walker M (July 1995). "Smoking cessation and the risk of stroke in middle-aged men". JAMA 274 (2): 155–60. doi:10.1001/jama.274.2.155. PMID 7596004.
^ Reynolds K, Lewis B, Nolen JD, et al. (February 2003). "Alcohol consumption and risk of stroke: a meta-analysis". JAMA 289 (5): 579–88. doi:10.1001/jama.289.5.579. PMID 12578491.
^ Sloan MA, Kittner SJ, Rigamonti D, Price TR (September 1991). "Occurrence of stroke associated with use/abuse of drugs". Neurology 41 (9): 1358–64. PMID 1891081.
^ American Heart Association. (2007). Stroke Risk Factors Americanheart.org. Retrieved on January 22, 2007.
^ Gorelick PB (1987). "Alcohol and stroke". Stroke; a Journal of Cerebral Circulation 18 (1): 268–71. PMID 3810763.
^ Westover AN, McBride S, Haley RW (April 2007). "Stroke in young adults who abuse amphetamines or cocaine: a population-based study of hospitalized patients". Archives of General Psychiatry 64 (4): 495–502. doi:10.1001/archpsyc.64.4.495. PMID 17404126.
^ Cantu C, Arauz A, Murillo-Bonilla LM, López M, Barinagarrementeria F (2003). "Stroke associated with sympathomimetics contained in over-the-counter cough and cold drugs". Stroke 34 (7): 1667–72. doi:10.1161/01.STR.0000075293.45936.FA. PMID 12791938.
^ Ezekowitz JA, Straus SE, Majumdar SR, McAlister FA (December 2003). "Stroke: strategies for primary prevention". American Family Physician 68 (12): 2379–86. PMID 14705756.
^ a b c d Ederle J, Brown MM (October 2006). "The evidence for medicine versus surgery for carotid stenosis". European Journal of Radiology 60 (1): 3–7. doi:10.1016/j.ejrad.2006.05.021. PMID 16920313.
^ Whisnant JP (1996). "Effectiveness versus efficacy of treatment of hypertension for stroke prevention". Neurology 46 (2): 301–7. PMID 8614485.
^ Collins R, Peto R, MacMahon S, et al. (1990). "Blood pressure, stroke, and coronary heart disease. Part 2, Short-term reductions in blood pressure: overview of randomised drug trials in their epidemiological context". Lancet 335 (8693): 827–38. doi:10.1016/0140-6736(90)90944-Z. PMID 1969567.
^ Psaty BM, Lumley T, Furberg CD, et al. (2003). "Health outcomes associated with various antihypertensive therapies used as first-line agents: a network meta-analysis". JAMA 289 (19): 2534–44. doi:10.1001/jama.289.19.2534. PMID 12759325.
^ a b "Cholesterol, diastolic blood pressure, and stroke: 13,000 strokes in 450,000 people in 45 prospective cohorts. Prospective studies collaboration". Lancet 346 (8991-8992): 1647–53. 1995. doi:10.1016/S0140-6736(95)92836-7. PMID 8551820.
^ Gueyffier F, Boissel JP, Boutitie F, et al. (1997). "Effect of antihypertensive treatment in patients having already suffered from stroke. Gathering the evidence. The INDANA (INdividual Data ANalysis of Antihypertensive intervention trials) Project Collaborators". Stroke 28 (12): 2557–62. PMID 9412649.
^ Gueyffier F, Bulpitt C, Boissel JP, et al. (1999). "Antihypertensive drugs in very old people: a subgroup meta-analysis of randomised controlled trials. INDANA Group". Lancet 353 (9155): 793–6. doi:10.1016/S0140-6736(98)08127-6. PMID 10459960.
^ Staessen JA, Gasowski J, Wang JG, et al. (2000). "Risks of untreated and treated isolated systolic hypertension in the elderly: meta-analysis of outcome trials". Lancet 355 (9207): 865–72. doi:10.1016/S0140-6736(99)07330-4. PMID 10752701.
^ Beckett NS, Peters R, Fletcher AE, et al. (2008). "Treatment of Hypertension in Patients 80 Years of Age or Older". N. Engl. J. Med. 358 (18): 1887. doi:10.1056/NEJMoa0801369. PMID 18378519.
^ a b Neal B, MacMahon S, Chapman N (2000). "Effects of ACE inhibitors, calcium antagonists, and other blood-pressure-lowering drugs: results of prospectively designed overviews of randomised trials. Blood Pressure Lowering Treatment Trialists' Collaboration". Lancet 356 (9246): 1955–64. doi:10.1016/S0140-6736(00)03307-9. PMID 11130523.
^ The Allhat Officers And Coordinators For The Allhat Collaborative Research Group, (2002). "Major outcomes in high-risk hypertensive patients randomized to angiotensin-converting enzyme inhibitor or calcium channel blocker vs diuretic: The Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT)". JAMA 288 (23): 2981–97. doi:10.1001/jama.288.23.2981. PMID 12479763.
^ Wolf PA, Abbott RD, Kannel WB (1987). "Atrial fibrillation: a major contributor to stroke in the elderly. The Framingham Study". Arch. Intern. Med. 147 (9): 1561–4. doi:10.1001/archinte.147.9.1561. PMID 3632164.
^ Fuster V, Rydén LE, Cannom DS, et al. (2006). "ACC/AHA/ESC 2006 Guidelines for the Management of Patients with Atrial Fibrillation: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Revise the 2001 Guidelines for the Management of Patients With Atrial Fibrillation): developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society". Circulation 114 (7): e257–354. doi:10.1161/CIRCULATIONAHA.106.177292. PMID 16908781.
^ Iso H, Jacobs DR, Wentworth D, Neaton JD, Cohen JD (1989). "Serum cholesterol levels and six-year mortality from stroke in 350,977 men screened for the multiple risk factor intervention trial". N. Engl. J. Med. 320 (14): 904–10. doi:10.1056/NEJM198904063201405. PMID 2619783.
^ a b O'Regan C, Wu P, Arora P, Perri D, Mills EJ (2008). "Statin therapy in stroke prevention: a meta-analysis involving 121,000 patients". Am. J. Med. 121 (1): 24–33. doi:10.1016/j.amjmed.2007.06.033. PMID 18187070.
^ Hebert PR, Gaziano JM, Hennekens CH (1995). "An overview of trials of cholesterol lowering and risk of stroke". Arch. Intern. Med. 155 (1): 50–5. doi:10.1001/archinte.155.1.50. PMID 7802520.
^ "Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33). UK Prospective Diabetes Study (UKPDS) Group". Lancet 352 (9131): 837–53. 1998. doi:10.1016/S0140-6736(98)07019-6. PMID 9742976.
^ Dormandy JA, Charbonnel B, Eckland DJ, et al. (2005). "Secondary prevention of macrovascular events in patients with type 2 diabetes in the PROactive Study (PROspective pioglitAzone Clinical Trial In macroVascular Events): a randomised controlled trial". Lancet 366 (9493): 1279–89. doi:10.1016/S0140-6736(05)67528-9. PMID 16214598.
^ Johnson ES, Lanes SF, Wentworth CE, Satterfield MH, Abebe BL, Dicker LW (1999). "A metaregression analysis of the dose-response effect of aspirin on stroke". Arch. Intern. Med. 159 (11): 1248–53. doi:10.1001/archinte.159.11.1248. PMID 10371234.
^ a b Hankey GJ, Sudlow CL, Dunbabin DW (2000). "Thienopyridine derivatives (ticlopidine, clopidogrel) versus aspirin for preventing stroke and other serious vascular events in high vascular risk patients". Cochrane Database Syst Rev (2): CD001246. doi:10.1002/14651858.CD001246. PMID 10796426.
^ Halkes PH, van Gijn J, Kappelle LJ, Koudstaal PJ, Algra A (2006). "Aspirin plus dipyridamole versus aspirin alone after cerebral ischaemia of arterial origin (ESPRIT): randomised controlled trial". Lancet 367 (9523): 1665–73. doi:10.1016/S0140-6736(06)68734-5. PMID 16714187.
^ Algra A; Halkes, PH; Van Gijn, J; Kappelle, LJ; Koudstaal, PJ; Algra, A (2007). "Medium intensity oral anticoagulants versus aspirin after cerebral ischaemia of arterial origin (ESPRIT): a randomised controlled trial". Lancet Neurol 6 (2): 115–24. doi:10.1016/S1474-4422(06)70685-8. PMID 17239798.
^ Hart RG, Halperin JL, McBride R, Benavente O, Man-Son-Hing M, Kronmal RA (2000). "Aspirin for the primary prevention of stroke and other major vascular events: meta-analysis and hypotheses". Arch. Neurol. 57 (3): 326–32. doi:10.1001/archneur.57.3.326. PMID 10714657.
^ Bartolucci AA, Howard G (2006). "Meta-analysis of data from the six primary prevention trials of cardiovascular events using aspirin". Am. J. Cardiol. 98 (6): 746–50. doi:10.1016/j.amjcard.2006.04.012. PMID 16950176.
^ Berger JS, Roncaglioni MC, Avanzini F, Pangrazzi I, Tognoni G, Brown DL (2006). "Aspirin for the primary prevention of cardiovascular events in women and men: a sex-specific meta-analysis of randomized controlled trials". JAMA 295 (3): 306–13. doi:10.1001/jama.295.3.306. PMID 16418466.
^ Yerman T, Gan WQ, Sin DD (2007). "The influence of gender on the effects of aspirin in preventing myocardial infarction". BMC Med 5: 29. doi:10.1186/1741-7015-5-29. PMID 17949479.
^ Rothwell PM, Eliasziw M, Gutnikov SA, et al. (2003). "Analysis of pooled data from the randomised controlled trials of endarterectomy for symptomatic carotid stenosis". Lancet 361 (9352): 107–16. doi:10.1016/S0140-6736(03)12228-3. PMID 12531577.
^ Ringleb PA, Chatellier G, Hacke W, et al. (2008). "Safety of endovascular treatment of carotid artery stenosis compared with surgical treatment: a meta-analysis". J. Vasc. Surg. 47 (2): 350–5. doi:10.1016/j.jvs.2007.10.035. PMID 18241759.
^ Ederle J, Featherstone RL, Brown MM (2007). "Percutaneous transluminal angioplasty and stenting for carotid artery stenosis". Cochrane Database Syst Rev (4): CD000515. doi:10.1002/14651858.CD000515.pub3. PMID 17943745.
^ Rothwell PM, Eliasziw M, Gutnikov SA, Warlow CP, Barnett HJ (2004). "Endarterectomy for symptomatic carotid stenosis in relation to clinical subgroups and timing of surgery". Lancet 363 (9413): 915–24. doi:10.1016/S0140-6736(04)15785-1. PMID 15043958.
^ Fairhead JF, Mehta Z, Rothwell PM (2005). "Population-based study of delays in carotid imaging and surgery and the risk of recurrent stroke". Neurology 65 (3): 371–5. doi:10.1212/01.wnl.0000170368.82460.b4. PMID 16087900.
^ U.S. Preventive Services Task Force (2007). "Screening for carotid artery stenosis: U.S. Preventive Services Task Force recommendation statement". Ann. Intern. Med. 147 (12): 854–9. PMID 18087056.
^ Halliday A, Mansfield A, Marro J, et al. (2004). "Prevention of disabling and fatal strokes by successful carotid endarterectomy in patients without recent neurological symptoms: randomised controlled trial". Lancet 363 (9420): 1491–502. doi:10.1016/S0140-6736(04)16146-1. PMID 15135594.
^ Chambers BR, Donnan GA (2005). "Carotid endarterectomy for asymptomatic carotid stenosis". Cochrane Database Syst Rev (4): CD001923. doi:10.1002/14651858.CD001923.pub2. PMID 16235289.
^ Spence JD; Lees, K.; Spence, J. D. (September 2006). "Nutrition and stroke prevention". Stroke 37 (9): 2430–5. doi:10.1161/01.STR.0000236633.40160.ee. PMID 16873712.
^ Wang X, Qin X, Demirtas H, et al. (2007). "Efficacy of folic acid supplementation in stroke prevention: a meta-analysis". Lancet 369 (9576): 1876–82. doi:10.1016/S0140-6736(07)60854-X. PMID 17544768.
^ Lonn E, Yusuf S, Arnold MJ, et al. (2006). "Homocysteine lowering with folic acid and B vitamins in vascular disease". N. Engl. J. Med. 354 (15): 1567–77. doi:10.1056/NEJMoa060900. PMID 16531613.
^ Toole JF, Malinow MR, Chambless LE, et al. (2004). "Lowering homocysteine in patients with ischemic stroke to prevent recurrent stroke, myocardial infarction, and death: the Vitamin Intervention for Stroke Prevention (VISP) randomized controlled trial". JAMA 291 (5): 565–75. doi:10.1001/jama.291.5.565. PMID 14762035.
^ http://www.heartscore.org
^ Saver JL (2006). "Time is brain - quantified". Stroke 37 (37): 263–6. doi:10.1161/01.STR.0000196957.55928.ab. PMID 16339467.
^ The National Institute Of Neurological Disorders And Stroke Rt-Pa Stroke Study Group, (1995). "Tissue plasminogen activator for acute ischemic stroke. The National Institute of Neurological Disorders and Stroke rt-PA Stroke Study Group". New England Journal of Medicine 333 (24): 1581–7. doi:10.1056/NEJM199512143332401. PMID 7477192.
^ The European Cooperative Acute Stroke Study (ECASS), (2008). "Thrombolysis with Alteplase 3 to 4.5 Hours after Acute Ischemic Stroke". New England Journal of Medicine 359 (13): 1317–1329. doi:10.1056/NEJMoa0804656. PMID 18815396.
^ Dubinsky, R; Lai SM (2006). "Mortality of stroke patients treated with thrombolysis: analysis of nationwide inpatient sample". Neurology 66 (11): 1742–1744. doi:10.1212/01.wnl.0000218306.35681.38. PMID 16769953.
^ "Position Statement on the Use of Intravenous Thrombolytic Therapy in the Treatment of Stroke". American Academy of Emergency Medicine. Retrieved 2008-01-25.
^ Lee M, Hong KS, Saver JL (May 2010). "Efficacy of intra-arterial fibrinolysis for acute ischemic stroke: meta-analysis of randomized controlled trials". Stroke 41 (5): 932–7. doi:10.1161/STROKEAHA.109.574335. PMID 20360549.
^ Flint AC, Duckwiler GR, Budzik RF, Liebeskind DS, Smith WS (2007). "Mechanical thrombectomy of intracranial internal carotid occlusion: pooled results of the MERCI and Multi MERCI Part I trials". Stroke 38 (4): 1274–80. doi:10.1161/01.STR.0000260187.33864.a7. PMID 17332445.
^ Smith WS, Sung G, Starkman S, et al. (2005). "Safety and efficacy of mechanical embolectomy in acute ischemic stroke: results of the MERCI trial". Stroke 36 (7): 1432–8. doi:10.1161/01.STR.0000171066.25248.1d. PMID 15961709.
^ Lutsep HL, Rymer MM, Nesbit GM (2008). "Vertebrobasilar revascularization rates and outcomes in the MERCI and multi-MERCI trials". J Stroke Cerebrovasc Dis 17 (2): 55–7. doi:10.1016/j.jstrokecerebrovasdis.2007.11.003. PMID 18346645.
^ Smith WS (June 1, 2006). "Safety of mechanical thrombectomy and intravenous tissue plasminogen activator in acute ischemic stroke. Results of the multi Mechanical Embolus Removal in Cerebral Ischemia (MERCI) trial, part I". AJNR Am J Neuroradiol 27 (6): 1177–82. PMID 16775259.
^ Smith WS, Sung G, Saver J, et al. (2008). "Mechanical thrombectomy for acute ischemic stroke: final results of the Multi MERCI trial". Stroke 39 (4): 1205–12. doi:10.1161/STROKEAHA.107.497115. PMID 18309168.
^ Derdeyn CP, Chimowitz MI (August 2007). "Angioplasty and stenting for atherosclerotic intracranial stenosis: rationale for a randomized clinical trial". Neuroimaging Clin. N. Am. 17 (3): 355–63, viii–ix. doi:10.1016/j.nic.2007.05.001. PMID 17826637.
^ Krieger DW, De Georgia MA, Abou-Chebl A, et al. (August 2001). "Cooling for acute ischemic brain damage (cool aid): an open pilot study of induced hypothermia in acute ischemic stroke". Stroke 32 (8): 1847–54. PMID 11486115.
^ Schwab S, Schwarz S, Spranger M, Keller E, Bertram M, Hacke W (December 1998). "Moderate hypothermia in the treatment of patients with severe middle cerebral artery infarction". Stroke 29 (12): 2461–6. PMID 9836751.
^ Hart RG, Pearce LA, Aguilar MI (2007). "Meta-analysis: antithrombotic therapy to prevent stroke in patients who have nonvalvular atrial fibrillation". Ann. Intern. Med. 146 (12): 857–67. PMID 17577005.
^ Paciaroni M, Agnelli G, Micheli S, Caso V (2007). "Efficacy and safety of anticoagulant treatment in acute cardioembolic stroke: a meta-analysis of randomized controlled trials". Stroke 38 (2): 423–30. doi:10.1161/01.STR.0000254600.92975.1f. PMID 17204681. ACP JC synopsis
^ a b Coffey C. Edward, Cummings Jeffrey L, Starkstein Sergio, Robinson Robert (2000). Stroke - the American Psychiatric Press Textbook of Geriatric Neuropsychiatry (Second ed.). Washington DC: American Psychiatric Press. pp. 601–617.
^ Stanford Hospital & Clinics. "Cardiovascular Diseases: Effects of Stroke". Retrieved 2005.
^ a b Senelick Richard C., Rossi, Peter W., Dougherty, Karla (1994). Living with Stroke: A Guide for Families. Contemporary Books, Chicago. ISBN 0809226073. OCLC 42835161 40856888 42835161.
^ a b Villarosa, Linda, Ed., Singleton, LaFayette, MD, Johnson, Kirk A. (1993). Black Health Library Guide to Stroke. Henry Holt and Company, New York.
^ Reith J, Jørgensen HS, Nakayama H, Raaschou HO, Olsen TS (August 1997). "Seizures in acute stroke: predictors and prognostic significance. The Copenhagen Stroke Study". Stroke 28 (8): 1585–9. PMID 9259753.
^ Burn J, Dennis M, Bamford J, Sandercock P, Wade D, Warlow C (December 1997). "Epileptic seizures after a first stroke: the Oxfordshire Community Stroke Project". BMJ 315 (7122): 1582–7. PMID 9437276. PMC 2127973.
^ Murray CJ, Lopez AD (1997). "Mortality by cause for eight regions of the world: Global Burden of Disease Study". Lancet 349 (9061): 1269–76. doi:10.1016/S0140-6736(96)07493-4. PMID 9142060.
^ (PDF) The World health report 2004. Annex Table 2: Deaths by cause, sex and mortality stratum in WHO regions, estimates for 2002.. Geneva: World Health Organization. 2004.
^ Ellekjær, H; Holmen J, Indredavik B, Terent A (November 1, 1997). "Epidemiology of Stroke in Innherred, Norway, 1994 to 1996 : Incidence and 30-Day Case-Fatality Rate". Stroke 28 (11): 2180–2184. PMID 9368561. Retrieved 2008-01-22.
^ Bongers T, de Maat M, van Goor M et al. (2006). "High von Willebrand factor levels increase the risk of first ischemic stroke: influence of ADAMTS13, inflammation, and genetic variability". Stroke 37 (11): 2672–7. doi:10.1161/01.STR.0000244767.39962.f7. PMID 16990571.
^ Ashrafian H (2010). "Familial stroke 2700 years ago". Stroke 41 (4): e187. PMID 20185778.
^ a b Thompson JE (August 1, 1996). "The evolution of surgery for the treatment and prevention of stroke. The Willis Lecture". Stroke 27 (8): 1427–34. PMID 8711815.
^ Kopito, Jeff (September 2001). "A Stroke in Time" ([dead link]). MERGINET.com 6 (9).
^ R. Barnhart, ed. The Barnhart Concise Dictionary of Etymology (1995)
^ Schiller F (April 1970). "Concepts of stroke before and after Virchow". Med Hist 14 (2): 115–31. PMID 4914683.
[edit]Further reading
J. P. Mohr, Dennis Choi, James Grotta, Philip Wolf (2004). Stroke: Pathophysiology, Diagnosis, and Management. New York: Churchill Livingstone. ISBN 0-443-06600-0. OCLC 52990861 50477349 52990861.
Charles P. Warlow, Jan van Gijn, Martin S. Dennis, Joanna M. Wardlaw, John M. Bamford, Graeme J. Hankey, Peter A. G. Sandercock, Gabriel Rinkel, Peter Langhorne, Cathie Sudlow, Peter Rothwell (2008). Stroke: Practical Management (3rd ed.). Wiley-Blackwell. ISBN 1-4051-2766-X.
[hide]
v • d • e
CNS disease, Vascular disease: Cerebrovascular diseases (G45-G46 and I60-I69, 430-438)
Brain ischemia/
cerebral infarction
(ischemic stroke/TIA)
TACI, PACI
precerebral: Carotid artery stenosis
cerebral: MCA · ACA · Amaurosis fugax
Moyamoya disease
POCI
precerebral: Anterior spinal artery syndrome · Vertebrobasilar insufficiency (Subclavian steal syndrome)
brainstem: medulla (Medial medullary syndrome, Lateral medullary syndrome) · pons (Medial pontine syndrome/Foville's, Lateral pontine syndrome/Millard-Gubler) · midbrain (Weber's, Benedikt, Claude's)
cerebral: PCA · Lacunar stroke · Thalamic syndrome
cerebellar
General
cerebral: Cerebral venous sinus thrombosis · CADASIL · Binswanger's disease · Transient global amnesia
Intracranial hemorrhage
(hemorrhagic stroke)
Extra-axial
Epidural · Subdural · Subarachnoid
Cerebral/Intra-axial
Intraventricular
Brainstem
Duret haemorrhage
Aneurysm
Cerebral aneurysm (Intracranial berry aneurysm, Charcot-Bouchard aneurysm)
Other/general
Cerebral vasculitis
M: CNS
anat(s,m,p,4,e,b,d,c,a,f,l,g)/phys/devp/cell
noco(m,d,e,h,v,s)/cong/tumr,sysi/epon,injr
proc,drug(N1A/2AB/C/3/4/7A/B/C/D)
M: VAS
anat(a:h,u,t,a,l,v:h,u,t,a,l)/phys/devp
noco/syva/cong/tumr, sysi/epon
proc, drug(C3,C4,C5,C9)
Stroke (CVA)-
Update and Revision s
Introduction
A stroke occurs when an artery to the brain becomes blocked or ruptures, resulting in death of an area of brain tissue (cerebral infarction) and causing sudden symptoms.
1. Most strokes are ischemic (usually due to blockage of an artery), but some are hemorrhagic (due to rupture of an artery).
2. Transient ischemic attacks resemble ischemic strokes except the symptoms resolve within 1 hour.
3. Symptoms occur suddenly and can include muscle weakness, paralysis, abnormal or lost sensation on one side of the body, difficulty speaking, confusion, problems with vision, dizziness, and loss of balance and coordination.
4. Diagnosis is based on symptoms, but imaging and blood tests are also done.
5. Recovery after a stroke depends on many factors, such the location and amount of damage, the person's age, and the presence of other disorders.
6. Controlling high blood pressure, high cholesterol levels, and high blood sugar levels and not smoking help prevent strokes.
7. Treatment may include drugs to make blood less likely to clot or to break up clots and sometimes surgery.
A stroke is called a cerebrovascular disorder because it affects the brain (cerebro-) and the blood vessels (vascular).
Supplying the Brain With Blood
Blood is supplied to the brain through two pairs of large arteries:
• Internal carotid arteries, which carry blood from the heart along the front of the neck
• Vertebral arteries, which carry blood from the heart along the back of the neck
Understanding the Pato- physiology of stroke
In the skull, the vertebral arteries unite to form the basilar artery (at the back of the head). The internal carotid arteries and the basilar artery divide into several branches, including the cerebral arteries. Some branches join to form a circle of arteries (circle of Willis) that connect the vertebral and internal carotid arteries. Other arteries branch off from the circle of Willis like roads from a traffic circle. The branches carry blood to all parts of the brain.
When the large arteries that supply the brain are blocked, some people have no symptoms or have only a small stroke. But others with the same sort of blockage have a massive ischemic stroke. Why? Part of the explanation is collateral arteries. Collateral arteries run between other arteries, providing extra connections.
Cerebral Arteries
These arteries include the circle of Willis and connections between the arteries that branch off from the circle. Some people are born with large collateral arteries, which can protect them from strokes. Then when one artery is blocked, blood flow continues through a collateral artery, sometimes preventing a stroke. Other people are born with small collateral arteries. Small collateral arteries may be unable to pass enough blood to the affected area, so a stroke results.
Protection against stroke
The body can also protect itself against strokes by growing new arteries. When blockages develop slowly and gradually (as occurs in atherosclerosis), new arteries may grow in time to keep the affected area of the brain supplied with blood and thus prevent a stroke. If a stroke has already occurred, growing new arteries can help prevent a second stroke (but cannot reverse damage that has been done).
Epidemiology
In Western countries, strokes are the third most common cause of death and the most common cause of disabling neurologic damage. In the United States, over 600,000 people have a stroke and about 160,000 die of stroke each year.
Older people
Strokes are much more common among older people than among younger adults, usually because the disorders that lead to strokes progress over time. Over two thirds of all strokes occur in people older than 65. Slightly more than 50% of all strokes occur in men, but more than 60% of deaths due to stroke occur in women, possibly because women are on average older when the stroke occurs. Blacks are more likely than whites to have a stroke and to die of it.
Types of Stroke (Ischemic 80%; and hemorrhagic, 20%)
Types: There are two types of strokes: ischemic and hemorrhagic. About 80% of strokes are ischemic—usually due to a blocked artery, often blocked by a blood clot. Brain cells, thus deprived of their blood supply, do not receive enough oxygen and glucose (a sugar), which are carried by blood.
Oxygen deprivation
The damage that results depends on how long brain cells are deprived of blood. If they are deprived for only a brief time, brain cells are stressed, but they may recover. If brain cells are deprived longer (but possibly for only several minutes), brain cells die, and some functions may be lost. However, in such cases, a different area of the brain can sometimes learn how to do the functions previously done by the damaged area.
Transient Ischemic Attacks (TIAs) - Ministrokes
Transient ischemic attacks (TIAs), sometimes called ministrokes, are often an early warning sign of an impending ischemic stroke. They are caused by a brief interruption of the blood supply to part of the brain. Because the blood supply is restored quickly, brain tissue may not die, as it does in a stroke
Hemorrhagic strokes..
The other 20% of strokes are hemorrhagic—due to bleeding in or around the brain. In this type of stroke, a blood vessel ruptures, interfering with normal blood flow and allowing blood to leak into brain tissue. Blood that comes into direct contact with brain tissue irritates the tissue and can cause scarring, leading to seizures.
Risk Factors: The major risk factors for both types of stroke are
1. Atherosclerosis (narrowing or blockage of arteries by patchy deposits of fatty material in the walls of arteries)
2. High cholesterol levels
3. High blood pressure
4. Diabetes
5. Smoking
Atherosclerosis is a more important risk factor for ischemic stroke, and high blood pressure is a more important risk factor for hemorrhagic stroke. These risk factors can be controlled to some extent.
Other risk factors include
1. Having relatives who have had a stroke
2. Consuming too much alcohol
3. Using cocaine or amphetamines
4. Having an abnormal heart rhythm called atrial fibrillation
5. Having inflamed blood vessels (vasculitis)
For hemorrhagic stroke, risk factors also include using anticoagulants, having a bulge (aneurysm) in arteries within the skull, and having an abnormal connection between arteries and veins (arteriovenous malformation).
Incidence
The incidence of strokes has declined in recent decades, mainly because people are more aware of the importance of controlling high blood pressure and high cholesterol levels and stopping cigarette smoking. Controlling these factors reduces the risk of atherosclerosis.
Symptoms
Symptoms of a stroke or transient ischemic attack occur suddenly. They vary depending on the precise location of the blockage or bleeding in the brain (Brain Dysfunction: Dysfunction by Location and Brain Dysfunction: When Specific Areas of the Brain Are Damaged ).
Each area of the brain is supplied by specific arteries. For example, if an artery supplying the area of the brain that controls the left leg's muscle movements is blocked, the leg becomes weak or paralyzed. If the area of the brain that senses touch in the right arm is damaged, sensation in the right arm is lost.
Early treatment
Because early treatment can help limit loss of function and sensation, everyone should know what the early symptoms of stroke are. People who have any of these symptoms should see a doctor immediately, even if the symptom goes away quickly.
Most strokes, whether ischemic or hemorrhagic, typically cause one or more of the following symptoms:
1. Sudden weakness or paralysis on one side of the body (for example, half of the face, one arm or leg, or all of one side)
2. Sudden loss of sensation or abnormal sensations on one side of the body
3. Sudden difficulty speaking, sometimes with slurred speech
4. Sudden confusion, with difficulty understanding speech
5. Sudden dimness, blurring, or loss of vision, particularly in one eye
6. Sudden dizziness or loss of balance and coordination, leading to falls
Symptoms of a transient ischemic attack are the same, but they usually disappear within minutes and rarely last more than 1 hour.
Why Strokes Affect Only One Side of the Body
Strokes usually damage only one side of the brain. Because nerves in the brain cross over to the other side of the body, symptoms appear on the side of the body opposite the damaged side of the brain.
Symptoms of a hemorrhagic stroke may also include the following:
1. Sudden severe headache
2. Nausea and vomiting
3. Temporary or persistent loss of consciousness
4. Very high blood pressure
Other symptoms that may occur early include problems with memory, thinking, attention, or learning. People may be unable to recognize parts of the body and may be unaware of the stroke's effects. The peripheral field of vision may be reduced, and hearing may be partially lost.
Dizziness and vertigo may develop or persist. Control of bowel or bladder function may be lost.
Later symptoms may include stiffening and spasms of the muscles (spasticity) and inability to control emotions. A stroke can cause depression, or people may feel depressed because of the stroke.
In most people who have had an ischemic stroke, loss of function is usually greatest immediately after the stroke occurs. However, in about 15 to 20%, the stroke is progressive, causing greatest loss of function after a day or two. In people who have had a hemorrhagic stroke, function usually is lost progressively over minutes to hours.
Over days to months, some function is usually regained because even though some brain cells die, others are only stressed and may recover. Also, certain areas of the brain can sometimes switch to the functions previously done by the damaged part—a characteristic called plasticity. However, the early effects of a stroke, including paralysis, can become permanent. Muscles that are not used usually become permanently spastic and stiff, and painful muscle spasms may occur.
Walking, swallowing, physically saying words clearly, and doing daily activities may remain difficult.
Various problems with memory, thinking, attention, learning, or controlling emotions may persist. Depression, impairments in hearing or vision, or vertigo may be continuing problems. Control of bowel or bladder function may be permanently impaired.
Complications: When a stroke is severe, the brain swells, increasing pressure within the skull. Increased pressure can damage the brain directly or indirectly by forcing the brain downward in the skull.
The brain may be forced through the rigid structures that separate the brain into compartments, resulting in a serious problem called herniation (see Head Injuries:Introduction ). The pressure affects the respiratory center in the lower part of the brain stem and can cause irregular breathing, loss of consciousness, coma, and death.
The symptoms caused by a stroke can lead to other problems. If swallowing is difficult, people may inhale food, fluids, or other particles from the mouth. Such inhalation (called aspiration) can cause aspiration pneumonia, which may be serious.
Difficulty swallowing can also interfere with eating, resulting in under nutrition and dehydration. Not being able to move can result in pressure sores, muscle loss, and the formation of blood clots in deep veins of the legs and groin (deep vein thrombosis). Clots can break off, travel through the bloodstream, and block an artery to a lung (pulmonary embolism). If bladder control is impaired, urinary tract infections are more likely to develop.
Diagnosis
Symptoms suggest the diagnosis, but tests are needed to help doctors determine the following:
1. Whether stroke has occurred
2. Whether it is ischemic or hemorrhagic
3. Whether immediate treatment is required
Computed tomography (CT–see Common Imaging Tests: Computed Tomography) or magnetic resonance imaging (MRI–see Common Imaging Tests: Magnetic Resonance Imaging) of the brain is done. These tests can detect most hemorrhagic strokes, except for some subarachnoid hemorrhages. These tests can also detect many ischemic strokes but sometimes not until several hours after symptoms appear. The blood sugar level is measured immediately because a low blood sugar level (hypoglycemia) can cause symptoms similar to those of stroke.
Doctors evaluate people who have had a stroke for problems that can contribute to or cause a stroke, such as infection, a low blood oxygen level, and dehydration, Tests are done as needed.
People are asked about depression. The ability to swallow is evaluated, sometimes with x-rays taken after a radiopaque dye such as barium is swallowed. Depending on the type of stroke, more tests are done to identify the cause.
Prognosis
Certain factors suggest that the outcome of a stroke is likely to be poor. Strokes that cause unconsciousness or that affect a large part of the left side of the brain (which is responsible for language) may be particularly grave.
In adults who have had an ischemic stroke, problems that remain after 6 months are likely to be permanent, but children continue to improve slowly for many months. Older people fare less well than younger people. For people who already have other serious disorders (such as dementia), recovery is more limited.
If a hemorrhagic stroke is not massive and pressure within the brain is not very high, the outcome is likely to be better after than that after an ischemic stroke. Blood (in a hemorrhagic stroke) does not damage brain tissue as much as an inadequate supply of oxygen (in an ischemic stroke) does.
Prevention
Preventing strokes is preferable to treating them. The main strategy for preventing a first stroke is managing the major risk factors. High blood pressure (see High Blood Pressure) and diabetes (see Diabetes Mellitus (DM): Diabetes Mellitus)should be controlled. Cholesterol levels should be measured and, if high, lowered to reduce the risk of atherosclerosis (see Cholesterol Disorders: Treatment).
Smoking and use of amphetamines or cocaine should be stopped, and alcohol should be limited to no more than 2 drinks a day. Exercising regularly and, if overweight, losing weight help people control high blood pressure, diabetes, and high cholesterol levels. Having regular checkups enables a doctor to identify risk factors for stroke so that they can be managed quickly.
If people have had an ischemic stroke, taking an antiplatelet drug can reduce the risk of another ischemic stroke. Antiplatelet drugs make platelets less likely to clump and form clots, a common cause of ischemic stroke. (Platelets are tiny cell-like particles in blood that help it clot in response to damaged blood vessels.)
Aspirin , one of the most effective antiplatelet drugs, is usually prescribed. One adult's tablet or 1 children's tablet (which is about one fourth the dose of an adult aspirin ) is taken each day. Either dose seems to prevent strokes about equally well.
Taking a combination tablet that contains a low dose of aspirin and dipyridamole (an antiplatelet drug) is slightly more effective than taking aspirin alone.
Clopidogrel , another antiplatelet drug, is also slightly more effective than aspirin alone. It may be given to people who cannot tolerate aspirin.
Some people are allergic to antiplatelet drugs or similar drugs and cannot take them. Also, people who have gastrointestinal bleeding should not take antiplatelet drugs.
If an ischemic stroke or a transient ischemic attack is due to blood clots originating in the heart, warfarin , an anticoagulant, may be given to inhibit blood clotting. Because taking warfarin and an antiplatelet drug or taking aspirin plus clopidogrel greatly increases the risk of bleeding, these drugs are rarely used together for stroke prevention.
Treatment
Anyone with symptoms of a stroke should seek medical attention immediately.
Doctors check the person's vital functions, such as heart rate, breathing, temperature, and blood pressure, to make sure they are adequate. If they are not, measures to correct them are taken immediately.
For example, if people are in a coma or unresponsive (as may result from brain herniation), mechanical ventilation (with a breathing tube inserted through the mouth or nose) may be needed to help them breathe.
If symptoms suggest that pressure within the skull is high, drugs may be given to reduce swelling in the brain, and a monitor may be put in the brain to periodically measure the pressure.
Other treatments used during the first hours depend on the type of stroke. These treatments include drugs (such as antiplatelet drugs, anticoagulants, drugs to break up clots, and drugs to control high blood pressure) and surgery to remove blood that has accumulated.
Later and ongoing treatments focus on preventing subsequent strokes, treating and preventing problems that strokes can cause, and helping people regain as much function as possible (rehabilitation).
Preventing and Treating Problems After a Stroke
Problem Measures
Blood clots in the legs To prevent blood clots, doctors may give anticoagulants, such as heparin or low molecular weight heparin, put elastic or air-filled support stockings on the person's legs to improve blood circulation, or both.Moving the legs, which improves blood flow, can also help. People, if able, are encouraged to walk or simply move their legs (for example, extending and flexing their ankles). If people cannot move their legs, a therapist or other staff member moves their legs for them (called passive exercise).
Pressure sores Nurses, other staff members, or caregivers should frequently turn or reposition people who are confined to a bed or wheelchair. Areas likely to develop pressures sores should be inspected every day.
Permanent shortening of muscles that limits movement (contractures) Moving the limbs can prevent contractures. People, if able, are encouraged to move and change positions regularly. Or a therapist or other staff member moves their limbs for them and makes sure the limbs are placed in appropriate resting positions. Sometimes splints are used to keep the limbs in place.
Difficulty swallowing People are evaluated for difficulty swallowing. If they have difficulty, care is taken to provide them with enough fluids and nourishment. Sometimes learning simple techniques (for example, how to position the head, how to breathe when swallowing) can help the person swallow safely. Tube feedings may be necessary until the ability to swallow returns.
Difficulty breathing If people smoke, they are encouraged to stop. Therapists also teach them to do deep breathing exercises and to cough to clear the airways. Therapists may provide a handheld breathing device. If needed, oxygen is provided through a face mask or a tube inserted in the nose or in the mouth.
Urinary tract infections If possible, a urinary catheter, which can cause urinary infections, is not used. If a catheter is needed, it is removed as soon as possible.
Discouragement and depression Doctors discuss the effects of the stroke with affected people and their family members or other caregivers. The discussion includes the type of recovery that can be expected and ways to cope with limitations of function. People and their caregivers are put in contact with stroke support groups. Formal counseling or drugs may be necessary to treat depression.
Rehabilitation: Intensive rehabilitation can help many people overcome disabilities after a stroke (see Rehabilitation: Brain Injuries). The exercises and training of rehabilitation encourage unaffected areas of the brain to learn to perform functions that were done by the damaged area. Also, people are taught new ways to use muscles unaffected by the stroke to compensate for losses in function.
The goals of rehabilitation are the following:
1. To regain as much normal function as possible
2. To maintain and improve physical condition
3. To help people relearn old skills and learn new ones as needed
Success depends on the area of the brain damaged and the person's general physical condition, functional and cognitive abilities before the stroke, social situation, learning ability, and attitude. Patience and perseverance are crucial. Participating actively in the rehabilitation program can help people avoid or lessen depression.
Rehabilitation is started in the hospital as soon as people are physically able—usually within 1 or 2 days of admission. After discharge from the hospital, rehabilitation can be continued on an outpatient basis, in a nursing home, in a rehabilitation center, or at home. Occupational and physical therapists can suggest ways to make life easier and the home safer for people with disabilities.
Family members and friends can contribute to a person's rehabilitation by keeping in mind what effects a stroke can have, so that they can better understand and support the person. Support groups can provide emotional encouragement and practical advice for people who have had a stroke and for those who care for them.
End-of-Life Issues
For some people who have had a stroke, quality of life is predicted to remain very poor despite treatment. For such people, care focuses on control of pain, comfort measures, and provision of fluids and nourishment. People who have had a stroke should establish advance directives (seeLegal and Ethical Issues: Advance Directives) as soon as possible because the recurrence and progression of strokes are unpredictable. Advance directives can help a doctor determine what kind of medical care people want if they become unable to make these decisions.
Notes and Comments
Stroke
Stroke
Classification and external resources
CT scan slice of the brain showing a right-hemispheric ischemic stroke (left side of image).
ICD-10 I61.-I64.
ICD-9 434.91
OMIM 601367
DiseasesDB 2247
MedlinePlus 000726
eMedicine neuro/9 emerg/558 emerg/557 pmr/187
MeSH D020521
A stroke, known medically as a cerebrovascular accident (CVA), is the rapidly developing loss of brain function(s) due to disturbance in the blood supply to the brain. This can be due to ischemia (lack of blood flow) caused by blockage (thrombosis, arterial embolism), or a hemorrhage (leakage of blood).[1] As a result, the affected area of the brain is unable to function, leading to inability to move one or more limbs on one side of the body, inability to understand or formulate speech, or an inability to see one side of the visual field.[2]
A stroke is a medical emergency and can cause permanent neurological damage, complications, and even death. It is the leading cause of adult disability in the United States and Europe and it is the number two cause of death worldwide.[3] Risk factors for stroke include advanced age, hypertension (high blood pressure), previous stroke or transient ischemic attack (TIA), diabetes, high cholesterol, cigarette smoking and atrial fibrillation.[4] High blood pressure is the most important modifiable risk factor of stroke.[2]
A stroke is occasionally treated in a hospital with thrombolysis (also known as a "clot buster"). Post-stroke prevention may involve the administration of antiplatelet drugs such as aspirin and dipyridamole, control and reduction of hypertension, the use of statins, and in selected patients with carotid endarterectomy, the use of anticoagulants.[2] Treatment to recover any lost function is stroke rehabilitation, involving health professions such as speech and language therapy, physical therapy and occupational therapy.
Contents [hide]
1 Definition
2 Classification
2.1 Ischemic stroke
2.2 Hemorrhagic stroke
3 Signs and symptoms
3.1 Early recognition
3.2 Subtypes
3.3 Associated symptoms
4 Causes
5 Pathophysiology
5.1 Ischemic
5.2 Hemorrhagic
6 Diagnosis
6.1 Physical examination
6.2 Imaging
6.3 Underlying etiology
7 Prevention
7.1 Risk factors
7.1.1 Blood pressure
7.1.2 Atrial fibrillation
7.1.3 Blood lipids
7.1.4 Diabetes mellitus
7.1.5 Anticoagulation drugs
7.1.6 Surgery
7.1.7 Nutritional and metabolic interventions
8 Treatment
8.1 Stroke unit
8.2 Treatment of ischemic stroke
8.2.1 Thrombolysis
8.2.2 Mechanical thrombectomy
8.2.3 Angioplasty and stenting
8.2.4 Therapeutic hypothermia
8.3 Secondary prevention of ischemic stroke
8.4 Treatment of hemorrhagic stroke
8.5 Care and rehabilitation
9 Prognosis
10 Epidemiology
11 History
12 References
13 Further reading
[edit]Definition
The traditional definition of stroke, devised by the World Health Organization in the 1970s,[5] is a "neurological deficit of cerebrovascular cause that persists beyond 24 hours or is interrupted by death within 24 hours". This definition was supposed to reflect the reversibility of tissue damage and was devised for the purpose, with the time frame of 24 hours being chosen arbitrarily. The 24-hour limit divides stroke from transient ischemic attack, which is a related syndrome of stroke symptoms that resolve completely within 24 hours.[2] With the availability of treatments that, when given early, can reduce stroke severity, many now prefer alternative concepts, such as brain attack and acute ischemic cerebrovascular syndrome (modeled after heart attack and acute coronary syndrome respectively), that reflect the urgency of stroke symptoms and the need to act swiftly.[6]
[edit]Classification
A slice of brain from the autopsy of a person who suffered an acute middle cerebral artery (MCA) stroke
Strokes can be classified into two major categories: ischemic and hemorrhagic.[7] Ischemic strokes are those that are caused by interruption of the blood supply, while hemorrhagic strokes are the ones which result from rupture of a blood vessel or an abnormal vascular structure. About 87% of strokes are caused by ischemia, and the remainder by hemorrhage. Some hemorrhages develop inside areas of ischemia ("hemorrhagic transformation"). It is unknown how many hemorrhages actually start as ischemic stroke.[2]
[edit]Ischemic stroke
Main articles: Cerebral infarction and Brain ischemia
In an ischemic stroke, blood supply to part of the brain is decreased, leading to dysfunction of the brain tissue in that area. There are four reasons why this might happen:
Thrombosis (obstruction of a blood vessel by a blood clot forming locally)
Embolism (obstruction due to an embolus from elsewhere in the body, see below),[2]
Systemic hypoperfusion (general decrease in blood supply, e.g. in shock)[8]
Venous thrombosis.[9]
Stroke without an obvious explanation is termed "cryptogenic" (of unknown origin); this constitutes 30-40% of all ischemic strokes.[2][10]
There are various classification systems for acute ischemic stroke. The Oxford Community Stroke Project classification (OCSP, also known as the Bamford or Oxford classification) relies primarily on the initial symptoms; based on the extent of the symptoms, the stroke episode is classified as total anterior circulation infarct (TACI), partial anterior circulation infarct (PACI), lacunar infarct (LACI) or posterior circulation infarct (POCI). These four entities predict the extent of the stroke, the area of the brain affected, the underlying cause, and the prognosis.[11][12] The TOAST (Trial of Org 10172 in Acute Stroke Treatment) classification is based on clinical symptoms as well as results of further investigations; on this basis, a stroke is classified as being due to (1) thrombosis or embolism due to atherosclerosis of a large artery, (2) embolism of cardiac origin, (3) occlusion of a small blood vessel, (4) other determined cause, (5) undetermined cause (two possible causes, no cause identified, or incomplete investigation).[2][13]
[edit]Hemorrhagic stroke
Main articles: Intracranial hemorrhage and intracerebral hemorrhage
CT scan showing an intracerebral hemorrhage with associated intraventricular hemorrhage.
Intracranial hemorrhage is the accumulation of blood anywhere within the skull vault. A distinction is made between intra-axial hemorrhage (blood inside the brain) and extra-axial hemorrhage (blood inside the skull but outside the brain). Intra-axial hemorrhage is due to intraparenchymal hemorrhage or intraventricular hemorrhage (blood in the ventricular system). The main types of extra-axial hemorrhage are epidural hematoma (bleeding between the dura mater and the skull), subdural hematoma (in the subdural space) and subarachnoid hemorrhage (between the arachnoid mater and pia mater). Most of the hemorrhagic stroke syndromes have specific symptoms (e.g. headache, previous head injury).
[edit]Signs and symptoms
Stroke symptoms typically start suddenly, over seconds to minutes, and in most cases do not progress further. The symptoms depend on the area of the brain affected. The more extensive the area of brain affected, the more functions that are likely to be lost. Some forms of stroke can cause additional symptoms. For example, in intracranial hemorrhage, the affected area may compress other structures. Most forms of stroke are not associated with headache, apart from subarachnoid hemorrhage and cerebral venous thrombosis and occasionally intracerebral hemorrhage.
[edit]Early recognition
Various systems have been proposed to increase recognition of stroke by patients, relatives and emergency first responders. A systematic review, updating a previous systematic review from 1994, looked at a number of trials to evaluate how well different physical examination findings are able to predict the presence or absence of stroke. It was found that sudden-onset face weakness, arm drift (e.g. if a person, when asked to raise both arms, involuntarily lets one arm drift downward) and abnormal speech are the findings most likely to lead to the correct identification of a case of stroke (+ likelihood ratio of 5.5 when at least one of these is present). Similarly, when all three of these are absent, the likelihood of stroke is significantly decreased (– likelihood ratio of 0.39).[14] While these findings are not perfect for diagnosing stroke, the fact that they can be evaluated relatively rapidly and easily make them very valuable in the acute setting.
Proposed systems include FAST (face, arm, speech, and time),[15] as advocated by the Department of Health (United Kingdom) and The Stroke Association, the American Stroke Association (www.strokeassociation.org) , National Stroke Association (US www.stroke.org), the Los Angeles Prehospital Stroke Screen (LAPSS)[16] and the Cincinnati Prehospital Stroke Scale (CPSS).[17] Use of these scales is recommended by professional guidelines.[18]
For people referred to the emergency room, early recognition of stroke is deemed important as this can expedite diagnostic tests and treatments. A scoring system called ROSIER (recognition of stroke in the emergency room) is recommended for this purpose; it is based on features from the medical history and physical examination.[18][19]
[edit]Subtypes
If the area of the brain affected contains one of the three prominent central nervous system pathways—the spinothalamic tract, corticospinal tract, and dorsal column (medial lemniscus), symptoms may include:
hemiplegia and muscle weakness of the face
numbness
reduction in sensory or vibratory sensation
In most cases, the symptoms affect only one side of the body (unilateral). Depending on the part of the brain affected, the defect in the brain is usually on the opposite side of the body. However, since these pathways also travel in the spinal cord and any lesion there can also produce these symptoms, the presence of any one of these symptoms does not necessarily indicate a stroke.
In addition to the above CNS pathways, the brainstem also consists of the 12 cranial nerves. A stroke affecting the brain stem therefore can produce symptoms relating to deficits in these cranial nerves:
altered smell, taste, hearing, or vision (total or partial)
drooping of eyelid (ptosis) and weakness of ocular muscles
decreased reflexes: gag, swallow, pupil reactivity to light
decreased sensation and muscle weakness of the face
balance problems and nystagmus
altered breathing and heart rate
weakness in sternocleidomastoid muscle with inability to turn head to one side
weakness in tongue (inability to protrude and/or move from side to side)
If the cerebral cortex is involved, the CNS pathways can again be affected, but also can produce the following symptoms:
aphasia (inability to speak or understand language from involvement of Broca's or Wernicke's area)
apraxia (altered voluntary movements)
visual field defect
memory deficits (involvement of temporal lobe)
hemineglect (involvement of parietal lobe)
disorganized thinking, confusion, hypersexual gestures (with involvement of frontal lobe)
anosognosia (persistent denial of the existence of a, usually stroke-related, deficit)
If the cerebellum is involved, the patient may have the following:
trouble walking
altered movement coordination
vertigo and or disequilibrium
[edit]Associated symptoms
Loss of consciousness, headache, and vomiting usually occurs more often in hemorrhagic stroke than in thrombosis because of the increased intracranial pressure from the leaking blood compressing on the brain.
If symptoms are maximal at onset, the cause is more likely to be a subarachnoid hemorrhage or an embolic stroke.
[edit]Causes
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Thrombotic stroke
In thrombotic stroke a thrombus (blood clot) usually forms around atherosclerotic plaques. Since blockage of the artery is gradual, onset of symptomatic thrombotic strokes is slower. A thrombus itself (even if non-occluding) can lead to an embolic stroke (see below) if the thrombus breaks off, at which point it is called an "embolus." Two types of thrombosis can cause stroke:
Large vessel disease involves the common and internal carotids, vertebral, and the Circle of Willis. Diseases that may form thrombi in the large vessels include (in descending incidence): atherosclerosis, vasoconstriction (tightening of the artery), aortic, carotid or vertebral artery dissection, various inflammatory diseases of the blood vessel wall (Takayasu arteritis, giant cell arteritis, vasculitis), noninflammatory vasculopathy, Moyamoya disease and fibromuscular dysplasia.
Small vessel disease involves the smaller arteries inside the brain: branches of the circle of Willis, middle cerebral artery, stem, and arteries arising from the distal vertebral and basilar artery. Diseases that may form thrombi in the small vessels include (in descending incidence): lipohyalinosis (build-up of fatty hyaline matter in the blood vessel as a result of high blood pressure and aging) and fibrinoid degeneration (stroke involving these vessels are known as lacunar infarcts) and microatheroma (small atherosclerotic plaques).
Sickle cell anemia, which can cause blood cells to clump up and block blood vessels, can also lead to stroke. A stroke is the second leading killer of people under 20 who suffer from sickle-cell anemia.[20]
Embolic stroke
An embolic stroke refers to the blockage of an artery by an arterial embolus, a travelling particle or debris in the arterial bloodstream originating from elsewhere. An embolus is most frequently a thrombus, but it can also be a number of other substances including fat (e.g. from bone marrow in a broken bone), air, cancer cells or clumps of bacteria (usually from infectious endocarditis).
Because an embolus arises from elsewhere, local therapy only solves the problem temporarily. Thus, the source of the embolus must be identified. Because the embolic blockage is sudden in onset, symptoms usually are maximal at start. Also, symptoms may be transient as the embolus is partially resorbed and moves to a different location or dissipates altogether.
Emboli most commonly arise from the heart (especially in atrial fibrillation) but may originate from elsewhere in the arterial tree. In paradoxical embolism, a deep vein thrombosis embolises through an atrial or ventricular septal defect in the heart into the brain.
Cardiac causes can be distinguished between high and low-risk:[21]
High risk: atrial fibrillation and paroxysmal atrial fibrillation, rheumatic disease of the mitral or aortic valve disease, artificial heart valves, known cardiac thrombus of the atrium or vertricle, sick sinus syndrome, sustained atrial flutter, recent myocardial infarction, chronic myocardial infarction together with ejection fraction <28 percent, symptomatic congestive heart failure with ejection fraction <30 percent, dilated cardiomyopathy, Libman-Sacks endocarditis, Marantic endocarditis, infective endocarditis, papillary fibroelastoma, left atrial myxoma and coronary artery bypass graft (CABG) surgery
Low risk/potential: calcification of the annulus (ring) of the mitral valve, patent foramen ovale (PFO), atrial septal aneurysm, atrial septal aneurysm with patent foramen ovale, left ventricular aneurysm without thrombus, isolated left atrial "smoke" on echocardiography (no mitral stenosis or atrial fibrillation), complex atheroma in the ascending aorta or proximal arch
Systemic hypoperfusion
Systemic hypoperfusion is the reduction of blood flow to all parts of the body. It is most commonly due to cardiac pump failure from cardiac arrest or arrhythmias, or from reduced cardiac output as a result of myocardial infarction, pulmonary embolism, pericardial effusion, or bleeding. Hypoxemia (low blood oxygen content) may precipitate the hypoperfusion. Because the reduction in blood flow is global, all parts of the brain may be affected, especially "watershed" areas - border zone regions supplied by the major cerebral arteries. A watershed stroke refers to the condition when blood supply to these areas is compromised. Blood flow to these areas does not necessarily stop, but instead it may lessen to the point where brain damage can occur. This phenomenon is also referred to as "last meadow" to point to the fact that in irrigation the last meadow receives the least amount of water.
Venous thrombosis
Cerebral venous sinus thrombosis leads to stroke due to locally increased venous pressure, which exceeds the pressure generated by the arteries. Infarcts are more likely to undergo hemorrhagic transformation (leaking of blood into the damaged area) than other types of ischemic stroke.[9]
Intracerebral hemorrhage
It generally occurs in small arteries or arterioles and is commonly due to hypertension, intracranial vascular malformations (including cavernous angiomas or arteriovenous malformations), cerebral amyloid angiopathy, or infarcts into which secondary haemorrhage has occurred.[2] Other potential causes are trauma, bleeding disorders, amyloid angiopathy, illicit drug use (e.g. amphetamines or cocaine). The hematoma enlarges until pressure from surrounding tissue limits its growth, or until it decompresses by emptying into the ventricular system, CSF or the pial surface. A third of intracerebral bleed is into the brain's ventricles. ICH has a mortality rate of 44 percent after 30 days, higher than ischemic stroke or even the very deadly subarachnoid hemorrhage (which, however, also may be classified as a type of stroke[2]).
[edit]Pathophysiology
[edit]Ischemic
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Ischemic stroke occurs due to a loss of blood supply to part of the brain, initiating the ischemic cascade.[22] Brain tissue ceases to function if deprived of oxygen for more than 60 to 90 seconds and after approximately three hours, will suffer irreversible injury possibly leading to death of the tissue, i.e., infarction. (This is why TPA's (e.g. Streptokinase, Altapase) are given only until three hours since the onset of the stroke.) Atherosclerosis may disrupt the blood supply by narrowing the lumen of blood vessels leading to a reduction of blood flow, by causing the formation of blood clots within the vessel, or by releasing showers of small emboli through the disintegration of atherosclerotic plaques. Embolic infarction occurs when emboli formed elsewhere in the circulatory system, typically in the heart as a consequence of atrial fibrillation, or in the carotid arteries, break off, enter the cerebral circulation, then lodge in and occlude brain blood vessels. Since blood vessels in the brain are now occluded, the brain becomes low in energy, and thus it resorts into using anaerobic respiration within the region of brain tissue affected by ischemia. Unfortunately, this kind of respiration produces less ATP but releases a by-product called lactic acid. Lactic acid is an irritant which could potentially destroy cells since it is an acid and disrupts the normal acid-bace balance in the brain. The ischemia area is referred to as the "ischemic penumbra".[23]
Then, as oxygen or glucose becomes depleted in ischemic brain tissue, the production of high energy phosphate compounds such as adenosine triphosphate (ATP) fails, leading to failure of energy-dependent processes (such as ion pumping) necessary for tissue cell survival. This sets off a series of interrelated events that result in cellular injury and death. A major cause of neuronal injury is release of the excitatory neurotransmitter glutamate. The concentration of glutamate outside the cells of the nervous system is normally kept low by so-called uptake carriers, which are powered by the concentration gradients of ions (mainly Na+) across the cell membrane. However, stroke cuts off the supply of oxygen and glucose which powers the ion pumps maintaining these gradients. As a result the transmembrane ion gradients run down, and glutamate transporters reverse their direction, releasing glutamate into the extracellular space. Glutamate acts on receptors in nerve cells (especially NMDA receptors), producing an influx of calcium which activates enzymes that digest the cells' proteins, lipids and nuclear material. Calcium influx can also lead to the failure of mitochondria, which can lead further toward energy depletion and may trigger cell death due to apoptosis.
Ischemia also induces production of oxygen free radicals and other reactive oxygen species. These react with and damage a number of cellular and extracellular elements. Damage to the blood vessel lining or endothelium is particularly important. In fact, many antioxidant neuroprotectants such as uric acid and NXY-059 work at the level of the endothelium and not in the brain per se. Free radicals also directly initiate elements of the apoptosis cascade by means of redox signaling.[20]
These processes are the same for any type of ischemic tissue and are referred to collectively as the ischemic cascade. However, brain tissue is especially vulnerable to ischemia since it has little respiratory reserve and is completely dependent on aerobic metabolism, unlike most other organs.
Brain tissue survival can be improved to some extent if one or more of these processes is inhibited. Drugs that scavenge reactive oxygen species, inhibit apoptosis, or inhibit excitatory neurotransmitters, for example, have been shown experimentally to reduce tissue injury due to ischemia. Agents that work in this way are referred to as being neuroprotective. Until recently, human clinical trials with neuroprotective agents have failed, with the probable exception of deep barbiturate coma. However, more recently NXY-059, the disulfonyl derivative of the radical-scavenging spintrap phenylbutylnitrone, is reported to be neuroprotective in stroke.[24] This agent appears to work at the level of the blood vessel lining or endothelium. Unfortunately, after producing favorable results in one large-scale clinical trial, a second trial failed to show favorable results.[20]
In addition to injurious effects on brain cells, ischemia and infarction can result in loss of structural integrity of brain tissue and blood vessels, partly through the release of matrix metalloproteases, which are zinc- and calcium-dependent enzymes that break down collagen, hyaluronic acid, and other elements of connective tissue. Other proteases also contribute to this process. The loss of vascular structural integrity results in a breakdown of the protective blood brain barrier that contributes to cerebral edema, which can cause secondary progression of the brain injury.
As is the case with any type of brain injury, the immune system is activated by cerebral infarction and may under some circumstances exacerbate the injury caused by the infarction. Inhibition of the inflammatory response has been shown experimentally to reduce tissue injury due to cerebral infarction, but this has not proved out in clinical studies.
[edit]Hemorrhagic
Head CT showing deep intracerebral hemorrhage due to bleeding within the cerebellum, approximately 30 hours old.
Hemorrhagic strokes result in tissue injury by causing compression of tissue from an expanding hematoma or hematomas. This can distort and injure tissue. In addition, the pressure may lead to a loss of blood supply to affected tissue with resulting infarction, and the blood released by brain hemorrhage appears to have direct toxic effects on brain tissue and vasculature.[20]
[edit]Diagnosis
Stroke is diagnosed through several techniques: a neurological examination (such as the Nihss), CT scans (most often without contrast enhancements) or MRI scans, Doppler ultrasound, and arteriography. The diagnosis of stroke itself is clinical, with assistance from the imaging techniques. Imaging techniques also assist in determining the subtypes and cause of stroke. There is yet no commonly used blood test for the stroke diagnosis itself, though blood tests may be of help in finding out the likely cause of stroke.[25]
[edit]Physical examination
A physical examination, including taking a medical history of the symptoms and a neurological status, helps giving an evaluation of the location and severity of a stroke. It can give a standard score on e.g. the NIH stroke scale.
[edit]Imaging
For diagnosing ischemic stroke in the emergency setting:[26]
CT scans (without contrast enhancements)
sensitivity= 16%
specificity= 96%
MRI scan
sensitivity= 83%
specificity= 98%
For diagnosing hemorrhagic stroke in the emergency setting:
CT scans (without contrast enhancements)
sensitivity= 89%
specificity= 100%
MRI scan
sensitivity= 81%
specificity= 100%
For detecting chronic hemorrhages, MRI scan is more sensitive.[27]
For the assessment of stable stroke, nuclear medicine scans SPECT and PET/CT may be helpful. SPECT documents cerebral blood flow and PET with FDG isotope the metabolic activity of the neurons.
[edit]Underlying etiology
When a stroke has been diagnosed, various other studies may be performed to determine the underlying etiology. With the current treatment and diagnosis options available, it is of particular importance to determine whether there is a peripheral source of emboli. Test selection may vary, since the cause of stroke varies with age, comorbidity and the clinical presentation. Commonly used techniques include:
an ultrasound/doppler study of the carotid arteries (to detect carotid stenosis) or dissection of the precerebral arteries
an electrocardiogram (ECG) and echocardiogram (to identify arrhythmias and resultant clots in the heart which may spread to the brain vessels through the bloodstream)
a Holter monitor study to identify intermittent arrhythmias
an angiogram of the cerebral vasculature (if a bleed is thought to have originated from an aneurysm or arteriovenous malformation)
blood tests to determine hypercholesterolemia, bleeding diathesis and some rarer causes such as homocysteinuria
[edit]Prevention
Given the disease burden of stroke, prevention is an important public health concern.[28] Primary prevention is less effective than secondary prevention (as judged by the number needed to treat to prevent one stroke per year).[28] Recent guidelines detail the evidence for primary prevention in stroke.[29] Because stroke may indicate underlying atherosclerosis, it is important to determine the patient's risk for other cardiovascular diseases such as coronary heart disease. Conversely, aspirin prevents against first stroke in patients who have suffered a myocardial infarction or patients with a high cardiovascular risk.[30][31]
[edit]Risk factors
The most important modifiable risk factors for stroke are high blood pressure and atrial fibrillation (although magnitude of this effect is small: the evidence from the Medical Research Council trials is that 833 patients have to be treated for 1 year to prevent one stroke[32][33]). Other modifiable risk factors include high blood cholesterol levels, diabetes, cigarette smoking[34][35] (active and passive), heavy alcohol consumption[36] and drug use,[37] lack of physical activity, obesity and unhealthy diet.[38] Alcohol use could predispose to ischemic stroke, and intracerebral and subarachnoid hemorrhage via multiple mechanisms (for example via hypertension, atrial fibrillation, rebound thrombocytosis and platelet aggregation and clotting disturbances).[39] The drugs most commonly associated with stroke are cocaine, amphetamines causing hemorrhagic stroke, but also over-the-counter cough and cold drugs containing sympathomimetics.[40][41]
No high quality studies have shown the effectiveness of interventions aimed at weight reduction, promotion of regular exercise, reducing alcohol consumption or smoking cessation.[42] Nonetheless, given the large body of circumstantial evidence, best medical management for stroke includes advice on diet, exercise, smoking and alcohol use.[43] Medication or drug therapy is the most common method of stroke prevention; carotid endarterectomy can be a useful surgical method of preventing stroke.
[edit]Blood pressure
Hypertension accounts for 35-50% of stroke risk.[44] Epidemiological studies suggest that even a small blood pressure reduction (5 to 6 mmHg systolic, 2 to 3 mmHg diastolic) would result in 40% fewer strokes.[45] Lowering blood pressure has been conclusively shown to prevent both ischemic and hemorrhagic strokes.[46][47] It is equally important in secondary prevention.[48] Even patients older than 80 years and those with isolated systolic hypertension benefit from antihypertensive therapy.[49][50][51] Studies show that intensive antihypertensive therapy results in a greater risk reduction.[52] The available evidence does not show large differences in stroke prevention between antihypertensive drugs —therefore, other factors such as protection against other forms of cardiovascular disease should be considered and cost.[52][53]
[edit]Atrial fibrillation
Patients with atrial fibrillation have a risk of 5% each year to develop stroke, and this risk is even higher in those with valvular atrial fibrillation.[54] Depending on the stroke risk, anticoagulation with medications such as coumarins or aspirin is warranted for stroke prevention.[55]
[edit]Blood lipids
High cholesterol levels have been inconsistently associated with (ischemic) stroke.[47][56] Statins have been shown to reduce the risk of stroke by about 15%.[57] Since earlier meta-analyses of other lipid-lowering drugs did not show a decreased risk,[58] statins might exert their effect through mechanisms other than their lipid-lowering effects.[57]
[edit]Diabetes mellitus
Patients with diabetes mellitus are 2 to 3 times more likely to develop stroke, and they commonly have hypertension and hyperlipidemia. Intensive disease control has been shown to reduce microvascular complications such as nephropathy and retinopathy but not macrovascular complications such as stroke.[59][60]
[edit]Anticoagulation drugs
Oral anticoagulants such as warfarin have been the mainstay of stroke prevention for over 50 years. However, several studies have shown that aspirin and antiplatelet drugs are highly effective in secondary prevention after a stroke or transient ischemic attack[30]. Low doses of aspirin (for example 75–150 mg) are as effective as high doses but have fewer side effects; the lowest effective dose remains unknown.[61] Thienopyridines (clopidogrel, ticlopidine) "might be slightly more effective" than aspirin and have a decreased risk of gastrointestinal bleeding, but they are more expensive.[62] Their exact role remains controversial. Ticlopidine has more skin rash, diarrhea, neutropenia and thrombotic thrombocytopenic purpura.[62] Dipyridamole can be added to aspirin therapy to provide a small additional benefit, even though headache is a common side effect.[63] Low-dose aspirin is also effective for stroke prevention after sustaining a myocardial infarction.[31] Oral anticoagulants are not advised for stroke prevention —any benefit is offset by bleeding risk.[64]
In primary prevention however, antiplatelet drugs did not reduce the risk of ischemic stroke while increasing the risk of major bleeding.[65][66] Further studies are needed to investigate a possible protective effect of aspirin against ischemic stroke in women.[67][68]
[edit]Surgery
Surgical procedures such as carotid endarterectomy or carotid angioplasty can be used to remove significant atherosclerotic narrowing (stenosis) of the carotid artery, which supplies blood to the brain. There is a large body of evidence supporting this procedure in selected cases.[43] Endarterectomy for a significant stenosis has been shown to be useful in the secondary prevention after a previous symptomatic stroke.[69] Carotid artery stenting has not been shown to be equally useful.[70][71] Patients are selected for surgery based on age, gender, degree of stenosis, time since symptoms and patients' preferences.[43] Surgery is most efficient when not delayed too long —the risk of recurrent stroke in a patient who has a 50% or greater stenosis is up to 20% after 5 years, but endarterectomy reduces this risk to around 5%. The number of procedures needed to cure one patient was 5 for early surgery (within two weeks after the initial stroke), but 125 if delayed longer than 12 weeks.[72][73]
Screening for carotid artery narrowing has not been shown to be a useful screening test in the general population.[74] Studies of surgical intervention for carotid artery stenosis without symptoms have shown only a small decrease in the risk of stroke.[75][76] To be beneficial, the complication rate of the surgery should be kept below 4%. Even then, for 100 surgeries, 5 patients will benefit by avoiding stroke, 3 will develop stroke despite surgery, 3 will develop stroke or die due to the surgery itself, and 89 will remain stroke-free but would also have done so without intervention.[43]
[edit]Nutritional and metabolic interventions
Nutrition, specifically the Mediterranean-style diet, has the potential of more than halving stroke risk.[77]
With regards to lowering homocysteine, a meta-analysis of previous trials has concluded that lowering homocysteine with folic acid and other supplements may reduce stroke risk.[78] However, the two largest randomized controlled trials included in the meta-analysis had conflicting results. One reported positve results;[79] whereas the other was negative.[80]
The European Society of Cardiology and the European Association for Cardiovascular Prevention and Rehabilitation have developed an interactive tool for prediction and managing the risk of heart attack and stroke in Europe. HeartScore is aimed at supporting clinicians in optimising individual cardiovascular risk reduction. The Heartscore Programme is available in 12 languages and offers web based or PC version [81].
[edit]Treatment
[edit]Stroke unit
Ideally, people who have had a stroke are admitted to a "stroke unit", a ward or dedicated area in hospital staffed by nurses and therapists with experience in stroke treatment. It has been shown that people admitted to a stroke unit have a higher chance of surviving than those admitted elsewhere in hospital, even if they are being cared for by doctors without experience in stroke.[2]
When an acute stroke is suspected by history and physical examination, the goal of early assessment is to determine the cause. Treatment varies according to the underlying cause of the stroke, thromboembolic (ischemic) or hemorrhagic. A non-contrast head CT scan can rapidly identify a hemorrhagic stroke by imaging bleeding in or around the brain. If no bleeding is seen, a presumptive diagnosis of ischemic stroke is made.
[edit]Treatment of ischemic stroke
An ischemic stroke is caused by a thrombus (blood clot) occluding blood flow to an artery supplying the brain. Definitive therapy is aimed at removing the blockage by breaking the clot down (thrombolysis), or by removing it mechanically (thrombectomy). The more rapidly blood flow is restored to the brain, the fewer brain cells die.[82]
Other medical therapies are aimed at minimizing clot enlargement or preventing new clots from forming. To this end, treatment with medications such as aspirin, clopidogrel and dipyridamole may be given to prevent platelets from aggregating[30].
In addition to definitive therapies, management of acute stroke includes control of blood sugars, ensuring the patient has adequate oxygenation and adequate intravenous fluids. Patients may be positioned with their heads flat on the stretcher, rather than sitting up, to increase blood flow to the brain. It is common for the blood pressure to be elevated immediately following a stroke. Although high blood pressure may cause some strokes, hypertension during acute stroke is desirable to allow adequate blood flow to the brain.
[edit]Thrombolysis
In increasing numbers of primary stroke centers, pharmacologic thrombolysis ("clot busting") with the drug tissue plasminogen activator (tPA), is used to dissolve the clot and unblock the artery. However, the use of tPA in acute stroke is controversial. On one hand, it is endorsed by the American Heart Association and the American Academy of Neurology as the recommended treatment for acute stroke within three hours of onset of symptoms as long as there are not other contraindications (such as abnormal lab values, high blood pressure, or recent surgery). This position for tPA is based upon the findings of two studies by one group of investigators[83] which showed that tPA improves the chances for a good neurological outcome. When administered within the first three hours, 39% of all patients who were treated with tPA had a good outcome at three months, only 26% of placebo controlled patients had a good functional outcome.
A recent study using alteplase for thrombolysis in ischemic stroke suggests clinical benefit with administration 3 to 4.5 hours after stroke onset.[84] However, in the NINDS trial 6.4% of patients with large strokes developed substantial brain hemorrhage as a complication from being given tPA. A recent study found the mortality to be higher among patients receiving tPA versus those who did not.[85] Additionally, it is the position of the American Academy of Emergency Medicine that objective evidence regarding the efficacy, safety, and applicability of tPA for acute ischemic stroke is insufficient to warrant its classification as standard of care.[86].
Intra-artial fibrinolysis, where a catherter is passed up an artery into the brain and the medication is injected at the site of thrombosis, has been found to improve outcomes in people with acute ischemic stroke.[87][original research?]
[edit]Mechanical thrombectomy
Merci Retriever L5.
Another intervention for acute ischemic stroke is removal of the offending thrombus directly. This is accomplished by inserting a catheter into the femoral artery, directing it into the cerebral circulation, and deploying a corkscrew-like device to ensnare the clot, which is then withdrawn from the body. Mechanical embolectomy devices have been demonstrated effective at restoring blood flow in patients who were unable to receive thrombolytic drugs or for whom the drugs were ineffective,[88][89][90][91] though no differences have been found between newer and older versions of the devices.[92] The devices have only been tested on patients treated with mechanical clot embolectomy within eight hours of the onset of symptoms.
[edit]Angioplasty and stenting
Angioplasty and stenting have begun to be looked at as possible viable options in treatment of acute ischemic stroke. In a systematic review of six uncontrolled, single-center trials, involving a total of 300 patients, of intra-cranial stenting in symptomatic intracranial arterial stenosis, the rate of technical success (reduction to stenosis of <50%) ranged from 90-98%, and the rate of major peri-procedural complications ranged from 4-10%. The rates of restenosis and/or stroke following the treatment were also favorable.[93] This data suggests that a large, randomized controlled trial is needed to more completely evaluate the possible therapeutic advantage of this treatment.
[edit]Therapeutic hypothermia
Main article: therapeutic hypothermia
Most of the data concerning therapeutic hypothermia’s effectiveness in treating ischemic stroke is limited to animal studies. These studies have focused primarily on ischemic as opposed to hemorrhagic stroke, as hypothermia has been associated with a lower clotting threshold. In these animal studies investigating the effect of temperature decline following ischemic stroke, hypothermia has been shown to be an effective all-purpose neuroprotectant.[94] This promising data has led to the initiation of a variety of human studies. At the time of this article’s publishing, this research has yet to return results. However, in terms of feasibility, the use of hypothermia to control intracranial pressure (ICP) after an ischemic stroke was found to be both safe and practical. The device used in this study was called the Arctic Sun.[95]
[edit]Secondary prevention of ischemic stroke
Anticoagulation can prevent recurrent stroke. Among patients with nonvalvular atrial fibrillation, anticoagulation can reduce stroke by 60% while antiplatelet agents can reduce stroke by 20%.[96]. However, a recent meta-analysis suggests harm from anti-coagulation started early after an embolic stroke.[97] Stroke prevention treatment for atrial fibrillation is determined according to the CHADS/CHADS2 system.
If studies show carotid stenosis, and the patient has residual function in the affected side, carotid endarterectomy (surgical removal of the stenosis) may decrease the risk of recurrence if performed rapidly after stroke.
[edit]Treatment of hemorrhagic stroke
Patients with intracerebral hemorrhage require neurosurgical evaluation to detect and treat the cause of the bleeding, although many may not need surgery. Anticoagulants and antithrombotics, key in treating ischemic stroke, can make bleeding worse and cannot be used in intracerebral hemorrhage. Patients are monitored and their blood pressure, blood sugar, and oxygenation are kept at optimum levels.
[edit]Care and rehabilitation
Stroke rehabilitation is the process by which patients with disabling strokes undergo treatment to help them return to normal life as much as possible by regaining and relearning the skills of everyday living. It also aims to help the survivor understand and adapt to difficulties, prevent secondary complications and educate family members to play a supporting role.
A rehabilitation team is usually multidisciplinary as it involves staff with different skills working together to help the patient. These include nursing staff, physiotherapy, occupational therapy, speech and language therapy, and usually a physician trained in rehabilitation medicine. Some teams may also include psychologists, social workers, and pharmacists since at least one third of the patients manifest post stroke depression. Validated instruments such as the Barthel scale may be used to assess the likelihood of a stroke patient being able to manage at home with or without support subsequent to discharge from hospital.
Good nursing care is fundamental in maintaining skin care, feeding, hydration, positioning, and monitoring vital signs such as temperature, pulse, and blood pressure. Stroke rehabilitation begins almost immediately.
For most stroke patients, physical therapy (PT) and occupational therapy (OT) are the cornerstones of the rehabilitation process, but in many countries Neurocognitive Rehabilitation is used, too. Often, assistive technology such as a wheelchair, walkers, canes, and orthosis may be beneficial. PT and OT have overlapping areas of working but their main attention fields are; PT involves re-learning functions as transferring, walking and other gross motor functions. OT focusses on exercises and training to help relearn everyday activities known as the Activities of daily living (ADLs) such as eating, drinking, dressing, bathing, cooking, reading and writing, and toileting. Speech and language therapy is appropriate for patients with problems understanding speech or written words, problems forming speech and problems with swallowing.
Patients may have particular problems, such as complete or partial inability to swallow, which can cause swallowed material to pass into the lungs and cause aspiration pneumonia. The condition may improve with time, but in the interim, a nasogastric tube may be inserted, enabling liquid food to be given directly into the stomach. If swallowing is still unsafe after a week, then a percutaneous endoscopic gastrostomy (PEG) tube is passed and this can remain indefinitely.
Stroke rehabilitation should be started as quickly as possible and can last anywhere from a few days to over a year. Most return of function is seen in the first few months, and then improvement falls off with the "window" considered officially by U.S. state rehabilitation units and others to be closed after six months, with little chance of further improvement. However, patients have been known to continue to improve for years, regaining and strengthening abilities like writing, walking, running, and talking. Daily rehabilitation exercises should continue to be part of the stroke patient's routine. Complete recovery is unusual but not impossible and most patients will improve to some extent : proper diet and exercise are known to help the brain to recover.
[edit]Prognosis
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Disability affects 75% of stroke survivors enough to decrease their employability.[98] Stroke can affect patients physically, mentally, emotionally, or a combination of the three. The results of stroke vary widely depending on size and location of the lesion.[99] Dysfunctions correspond to areas in the brain that have been damaged.
Some of the physical disabilities that can result from stroke include muscle weakness, numbness, pressure sores, pneumonia, incontinence, apraxia (inability to perform learned movements), difficulties carrying out daily activities, appetite loss, speech loss, vision loss, and pain. If the stroke is severe enough, or in a certain location such as parts of the brainstem, coma or death can result.
Emotional problems resulting from stroke can result from direct damage to emotional centers in the brain or from frustration and difficulty adapting to new limitations. Post-stroke emotional difficulties include anxiety, panic attacks, flat affect (failure to express emotions), mania, apathy, and psychosis.
30 to 50% of stroke survivors suffer post stroke depression, which is characterized by lethargy, irritability, sleep disturbances, lowered self esteem, and withdrawal.[100] Depression can reduce motivation and worsen outcome, but can be treated with antidepressants.
Emotional lability, another consequence of stroke, causes the patient to switch quickly between emotional highs and lows and to express emotions inappropriately, for instance with an excess of laughing or crying with little or no provocation. While these expressions of emotion usually correspond to the patient's actual emotions, a more severe form of emotional lability causes patients to laugh and cry pathologically, without regard to context or emotion.[98] Some patients show the opposite of what they feel, for example crying when they are happy.[101] Emotional lability occurs in about 20% of stroke patients.
Cognitive deficits resulting from stroke include perceptual disorders, speech problems, dementia, and problems with attention and memory. A stroke sufferer may be unaware of his or her own disabilities, a condition called anosognosia. In a condition called hemispatial neglect, a patient is unable to attend to anything on the side of space opposite to the damaged hemisphere.
Up to 10% of all stroke patients develop seizures, most commonly in the week subsequent to the event; the severity of the stroke increases the likelihood of a seizure.[102][103]
[edit]Epidemiology
Stroke could soon be the most common cause of death worldwide.[104] Stroke is currently the second leading cause of death in the Western world, ranking after heart disease and before cancer,[2] and causes 10% of deaths worldwide.[105] Geographic disparities in stroke incidence have been observed, including the existence of a "stroke belt" in the southeastern United States, but causes of these disparities have not been explained.
The incidence of stroke increases exponentially from 30 years of age, and etiology varies by age.[106] Advanced age is one of the most significant stroke risk factors. 95% of strokes occur in people age 45 and older, and two-thirds of strokes occur in those over the age of 65.[100][20] A person's risk of dying if he or she does have a stroke also increases with age. However, stroke can occur at any age, including in fetuses.
Family members may have a genetic tendency for stroke or share a lifestyle that contributes to stroke. Higher levels of Von Willebrand factor are more common amongst people who have had ischemic stroke for the first time.[107] The results of this study found that the only significant genetic factor was the person's blood type. Having had a stroke in the past greatly increases one's risk of future strokes.
Men are 25% more likely to suffer strokes than women,[20] yet 60% of deaths from stroke occur in women.[101] Since women live longer, they are older on average when they have their strokes and thus more often killed (NIMH 2002).[20] Some risk factors for stroke apply only to women. Primary among these are pregnancy, childbirth, menopause and the treatment thereof (HRT).
[edit]History
Hippocrates first described the sudden paralysis that is often associated with stroke.
Episodes of stroke and familial stroke have been reported from the 2nd millenium BC onward in ancient Mesopotamia and Persia[108]. Hippocrates (460 to 370 BC) was first to describe the phenomenon of sudden paralysis that is often associated with ischemia. Apoplexy, from the Greek word meaning "struck down with violence,” first appeared in Hippocratic writings to describe this phenomenon.[109][110]
The word stroke was used as a synonym for apoplectic seizure as early as 1599,[111] and is a fairly literal translation of the Greek term.
In 1658, in his Apoplexia, Johann Jacob Wepfer (1620–1695) identified the cause of hemorrhagic stroke when he suggested that people who had died of apoplexy had bleeding in their brains.[109][20] Wepfer also identified the main arteries supplying the brain, the vertebral and carotid arteries, and identified the cause of ischemic stroke [also known as cerebral infarction] when he suggested that apoplexy might be caused by a blockage to those vessels.[20]
Rudolf Virchow first described the mechanism of thromboembolism as a major factor.[112]
[edit]References
^ Sims NR, Muyderman H (September 2009). "Mitochondria, oxidative metabolism and cell death in stroke". Biochimica et Biophysica Acta 1802 (1): 80–91. doi:10.1016/j.bbadis.2009.09.003. PMID 19751827.
^ a b c d e f g h i j k l Donnan GA, Fisher M, Macleod M, Davis SM (May 2008). "Stroke". Lancet 371 (9624): 1612–23. doi:10.1016/S0140-6736(08)60694-7. PMID 18468545.
^ Feigin VL (2005). "Stroke epidemiology in the developing world". Lancet 365 (9478): 2160–1. doi:10.1016/S0140-6736(05)66755-4. PMID 15978910.
^ Stroke Mount Sinai Hospital, New York
^ World Health Organisation (1978). Cerebrovascular Disorders (Offset Publications). Geneva: World Health Organization. ISBN 9241700432. OCLC 4757533.
^ Kidwell CS, Warach S (December 2003). "Acute ischemic cerebrovascular syndrome: diagnostic criteria". Stroke 34 (12): 2995–8. doi:10.1161/01.STR.0000098902.69855.A9. PMID 14605325.
^ "Brain Basics: Preventing Stroke". National Institute of Neurological Disorders and Stroke. Retrieved 2009-10-24.
^ Shuaib A, Hachinski VC (September 1991). "Mechanisms and management of stroke in the elderly". CMAJ 145 (5): 433–43. PMID 1878825.
^ a b Stam J (April 2005). "Thrombosis of the cerebral veins and sinuses". The New England Journal of Medicine 352 (17): 1791–8. doi:10.1056/NEJMra042354. PMID 15858188.
^ Guercini F, Acciarresi M, Agnelli G, Paciaroni M (April 2008). "Cryptogenic stroke: time to determine aetiology". Journal of Thrombosis and Haemostasis 6 (4): 549–54. doi:10.1111/j.1538-7836.2008.02903.x. PMID 18208534.
^ Bamford J, Sandercock P, Dennis M, Burn J, Warlow C (June 1991). "Classification and natural history of clinically identifiable subtypes of cerebral infarction". Lancet 337 (8756): 1521–6. doi:10.1016/0140-6736(91)93206-O. PMID 1675378. Later publications distinguish between "syndrome" and "infarct", based on evidence from imaging. "Syndrome" may be replaced by "hemorrhage" if imaging demonstrates a bleed. See Internet Stroke Center. "Oxford Stroke Scale". Retrieved 2008-11-14.
^ Bamford JM (2000). "The role of the clinical examination in the subclassification of stroke". Cerebrovascular Diseases 10 Suppl 4: 2–4. doi:10.1159/000047582. PMID 11070389.
^ Adams HP, Bendixen BH, Kappelle LJ, et al. (January 1993). "Classification of subtype of acute ischemic stroke. Definitions for use in a multicenter clinical trial. TOAST. Trial of Org 10172 in Acute Stroke Treatment". Stroke 24 (1): 35–41. PMID 7678184.
^ Goldstein LB, Simel DL (May 2005). "Is this patient having a stroke?". JAMA 293 (19): 2391–402. doi:10.1001/jama.293.19.2391. PMID 15900010.
^ Harbison J, Massey A, Barnett L, Hodge D, Ford GA (June 1999). "Rapid ambulance protocol for acute stroke". Lancet 353 (9168): 1935. doi:10.1016/S0140-6736(99)00966-6. PMID 10371574.
^ Kidwell CS, Saver JL, Schubert GB, Eckstein M, Starkman S (1998). "Design and retrospective analysis of the Los Angeles Prehospital Stroke Screen (LAPSS)". Prehospital Emergency Care 2 (4): 267–73. doi:10.1080/10903129808958878. PMID 9799012.
^ Kothari RU, Pancioli A, Liu T, Brott T, Broderick J (April 1999). "Cincinnati Prehospital Stroke Scale: reproducibility and validity". Annals of Emergency Medicine 33 (4): 373–8. doi:10.1016/S0196-0644(99)70299-4. PMID 10092713.
^ a b National Institute for Health and Clinical Excellence. Clinical guideline 68: Stroke. London, 2008.
^ Nor AM, Davis J, Sen B, et al. (November 2005). "The Recognition of Stroke in the Emergency Room (ROSIER) scale: development and validation of a stroke recognition instrument". Lancet Neurology 4 (11): 727–34. doi:10.1016/S1474-4422(05)70201-5. PMID 16239179.
^ a b c d e f g h i National Institute of Neurological Disorders and Stroke (NINDS) (1999). "Stroke: Hope Through Research". National Institutes of Health.
^ Ay H, Furie KL, Singhal A, Smith WS, Sorensen AG, Koroshetz WJ (November 2005). "An evidence-based causative classification system for acute ischemic stroke". Annals of Neurology 58 (5): 688–97. doi:10.1002/ana.20617. PMID 16240340.
^ Deb P, Sharma S, Hassan KM. "Pathophysiologic mechanisms of acute ischemic stroke: An overview with emphasis on therapeutic significance beyond thrombolysis". Pathophysiology. January 12, 2010. PMID 20074922.
^ Brunner and Suddarth's Textbook on Medical-Surgical Nursing, 11th Edition
^ Lees KR, Zivin JA, Ashwood T, et al. (February 2006). "NXY-059 for acute ischemic stroke". The New England Journal of Medicine 354 (6): 588–600. doi:10.1056/NEJMoa052980. PMID 16467546.
^ Hill MD (November 2005). "Diagnostic biomarkers for stroke: a stroke neurologist's perspective". Clinical Chemistry 51 (11): 2001–2. doi:10.1373/clinchem.2005.056382. PMID 16244286.
^ Chalela JA, Kidwell CS, Nentwich LM, et al. (January 2007). "Magnetic resonance imaging and computed tomography in emergency assessment of patients with suspected acute stroke: a prospective comparison". Lancet 369 (9558): 293–8. doi:10.1016/S0140-6736(07)60151-2. PMID 17258669.
^ Kidwell CS, Chalela JA, Saver JL, et al. (October 2004). "Comparison of MRI and CT for detection of acute intracerebral hemorrhage". JAMA 292 (15): 1823–30. doi:10.1001/jama.292.15.1823. PMID 15494579.
^ a b Straus SE, Majumdar SR, McAlister FA (September 2002). "New evidence for stroke prevention: scientific review". JAMA 288 (11): 1388–95. doi:10.1001/jama.288.11.1388. PMID 12234233.
^ Goldstein LB, Adams R, Alberts MJ, et al. (June 2006). "Primary prevention of ischemic stroke: a guideline from the American Heart Association/American Stroke Association Stroke Council: cosponsored by the Atherosclerotic Peripheral Vascular Disease Interdisciplinary Working Group; Cardiovascular Nursing Council; Clinical Cardiology Council; Nutrition, Physical Activity, and Metabolism Council; and the Quality of Care and Outcomes Research Interdisciplinary Working Group: the American Academy of Neurology affirms the value of this guideline". Stroke 37 (6): 1583–633. doi:10.1161/01.STR.0000223048.70103.F1. PMID 16675728.
^ a b c NPS Prescribing Practice Review 44: Antiplatelets and anticoagulants in stroke prevention (2009). Available at http://www.nps.org.au/health_professionals/publications/prescribing_practice_review/current/nps_prescribing_practice_review_44
^ a b Antithrombotic Trialists' Collaboration (January 2002). "Collaborative meta-analysis of randomised trials of antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high risk patients". BMJ 324 (7329): 71–86. doi:10.1136/bmj.324.7329.71. PMID 11786451.
^ "MRC trial of treatment of mild hypertension: principal results. Medical Research Council Working Party". British Medical Journal 291 (6488): 97–104. July 1985. doi:10.1136/bmj.291.6488.97. PMID 2861880.
^ Thomson R (2009). "Evidence based implementation of complex interventions". BMJ 339: b3124. doi:10.1136/bmj.b3124. PMID 19675081.
^ Hankey GJ (August 1999). "Smoking and risk of stroke". Journal of Cardiovascular Risk 6 (4): 207–11. PMID 10501270.
^ Wannamethee SG, Shaper AG, Whincup PH, Walker M (July 1995). "Smoking cessation and the risk of stroke in middle-aged men". JAMA 274 (2): 155–60. doi:10.1001/jama.274.2.155. PMID 7596004.
^ Reynolds K, Lewis B, Nolen JD, et al. (February 2003). "Alcohol consumption and risk of stroke: a meta-analysis". JAMA 289 (5): 579–88. doi:10.1001/jama.289.5.579. PMID 12578491.
^ Sloan MA, Kittner SJ, Rigamonti D, Price TR (September 1991). "Occurrence of stroke associated with use/abuse of drugs". Neurology 41 (9): 1358–64. PMID 1891081.
^ American Heart Association. (2007). Stroke Risk Factors Americanheart.org. Retrieved on January 22, 2007.
^ Gorelick PB (1987). "Alcohol and stroke". Stroke; a Journal of Cerebral Circulation 18 (1): 268–71. PMID 3810763.
^ Westover AN, McBride S, Haley RW (April 2007). "Stroke in young adults who abuse amphetamines or cocaine: a population-based study of hospitalized patients". Archives of General Psychiatry 64 (4): 495–502. doi:10.1001/archpsyc.64.4.495. PMID 17404126.
^ Cantu C, Arauz A, Murillo-Bonilla LM, López M, Barinagarrementeria F (2003). "Stroke associated with sympathomimetics contained in over-the-counter cough and cold drugs". Stroke 34 (7): 1667–72. doi:10.1161/01.STR.0000075293.45936.FA. PMID 12791938.
^ Ezekowitz JA, Straus SE, Majumdar SR, McAlister FA (December 2003). "Stroke: strategies for primary prevention". American Family Physician 68 (12): 2379–86. PMID 14705756.
^ a b c d Ederle J, Brown MM (October 2006). "The evidence for medicine versus surgery for carotid stenosis". European Journal of Radiology 60 (1): 3–7. doi:10.1016/j.ejrad.2006.05.021. PMID 16920313.
^ Whisnant JP (1996). "Effectiveness versus efficacy of treatment of hypertension for stroke prevention". Neurology 46 (2): 301–7. PMID 8614485.
^ Collins R, Peto R, MacMahon S, et al. (1990). "Blood pressure, stroke, and coronary heart disease. Part 2, Short-term reductions in blood pressure: overview of randomised drug trials in their epidemiological context". Lancet 335 (8693): 827–38. doi:10.1016/0140-6736(90)90944-Z. PMID 1969567.
^ Psaty BM, Lumley T, Furberg CD, et al. (2003). "Health outcomes associated with various antihypertensive therapies used as first-line agents: a network meta-analysis". JAMA 289 (19): 2534–44. doi:10.1001/jama.289.19.2534. PMID 12759325.
^ a b "Cholesterol, diastolic blood pressure, and stroke: 13,000 strokes in 450,000 people in 45 prospective cohorts. Prospective studies collaboration". Lancet 346 (8991-8992): 1647–53. 1995. doi:10.1016/S0140-6736(95)92836-7. PMID 8551820.
^ Gueyffier F, Boissel JP, Boutitie F, et al. (1997). "Effect of antihypertensive treatment in patients having already suffered from stroke. Gathering the evidence. The INDANA (INdividual Data ANalysis of Antihypertensive intervention trials) Project Collaborators". Stroke 28 (12): 2557–62. PMID 9412649.
^ Gueyffier F, Bulpitt C, Boissel JP, et al. (1999). "Antihypertensive drugs in very old people: a subgroup meta-analysis of randomised controlled trials. INDANA Group". Lancet 353 (9155): 793–6. doi:10.1016/S0140-6736(98)08127-6. PMID 10459960.
^ Staessen JA, Gasowski J, Wang JG, et al. (2000). "Risks of untreated and treated isolated systolic hypertension in the elderly: meta-analysis of outcome trials". Lancet 355 (9207): 865–72. doi:10.1016/S0140-6736(99)07330-4. PMID 10752701.
^ Beckett NS, Peters R, Fletcher AE, et al. (2008). "Treatment of Hypertension in Patients 80 Years of Age or Older". N. Engl. J. Med. 358 (18): 1887. doi:10.1056/NEJMoa0801369. PMID 18378519.
^ a b Neal B, MacMahon S, Chapman N (2000). "Effects of ACE inhibitors, calcium antagonists, and other blood-pressure-lowering drugs: results of prospectively designed overviews of randomised trials. Blood Pressure Lowering Treatment Trialists' Collaboration". Lancet 356 (9246): 1955–64. doi:10.1016/S0140-6736(00)03307-9. PMID 11130523.
^ The Allhat Officers And Coordinators For The Allhat Collaborative Research Group, (2002). "Major outcomes in high-risk hypertensive patients randomized to angiotensin-converting enzyme inhibitor or calcium channel blocker vs diuretic: The Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT)". JAMA 288 (23): 2981–97. doi:10.1001/jama.288.23.2981. PMID 12479763.
^ Wolf PA, Abbott RD, Kannel WB (1987). "Atrial fibrillation: a major contributor to stroke in the elderly. The Framingham Study". Arch. Intern. Med. 147 (9): 1561–4. doi:10.1001/archinte.147.9.1561. PMID 3632164.
^ Fuster V, Rydén LE, Cannom DS, et al. (2006). "ACC/AHA/ESC 2006 Guidelines for the Management of Patients with Atrial Fibrillation: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Revise the 2001 Guidelines for the Management of Patients With Atrial Fibrillation): developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society". Circulation 114 (7): e257–354. doi:10.1161/CIRCULATIONAHA.106.177292. PMID 16908781.
^ Iso H, Jacobs DR, Wentworth D, Neaton JD, Cohen JD (1989). "Serum cholesterol levels and six-year mortality from stroke in 350,977 men screened for the multiple risk factor intervention trial". N. Engl. J. Med. 320 (14): 904–10. doi:10.1056/NEJM198904063201405. PMID 2619783.
^ a b O'Regan C, Wu P, Arora P, Perri D, Mills EJ (2008). "Statin therapy in stroke prevention: a meta-analysis involving 121,000 patients". Am. J. Med. 121 (1): 24–33. doi:10.1016/j.amjmed.2007.06.033. PMID 18187070.
^ Hebert PR, Gaziano JM, Hennekens CH (1995). "An overview of trials of cholesterol lowering and risk of stroke". Arch. Intern. Med. 155 (1): 50–5. doi:10.1001/archinte.155.1.50. PMID 7802520.
^ "Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33). UK Prospective Diabetes Study (UKPDS) Group". Lancet 352 (9131): 837–53. 1998. doi:10.1016/S0140-6736(98)07019-6. PMID 9742976.
^ Dormandy JA, Charbonnel B, Eckland DJ, et al. (2005). "Secondary prevention of macrovascular events in patients with type 2 diabetes in the PROactive Study (PROspective pioglitAzone Clinical Trial In macroVascular Events): a randomised controlled trial". Lancet 366 (9493): 1279–89. doi:10.1016/S0140-6736(05)67528-9. PMID 16214598.
^ Johnson ES, Lanes SF, Wentworth CE, Satterfield MH, Abebe BL, Dicker LW (1999). "A metaregression analysis of the dose-response effect of aspirin on stroke". Arch. Intern. Med. 159 (11): 1248–53. doi:10.1001/archinte.159.11.1248. PMID 10371234.
^ a b Hankey GJ, Sudlow CL, Dunbabin DW (2000). "Thienopyridine derivatives (ticlopidine, clopidogrel) versus aspirin for preventing stroke and other serious vascular events in high vascular risk patients". Cochrane Database Syst Rev (2): CD001246. doi:10.1002/14651858.CD001246. PMID 10796426.
^ Halkes PH, van Gijn J, Kappelle LJ, Koudstaal PJ, Algra A (2006). "Aspirin plus dipyridamole versus aspirin alone after cerebral ischaemia of arterial origin (ESPRIT): randomised controlled trial". Lancet 367 (9523): 1665–73. doi:10.1016/S0140-6736(06)68734-5. PMID 16714187.
^ Algra A; Halkes, PH; Van Gijn, J; Kappelle, LJ; Koudstaal, PJ; Algra, A (2007). "Medium intensity oral anticoagulants versus aspirin after cerebral ischaemia of arterial origin (ESPRIT): a randomised controlled trial". Lancet Neurol 6 (2): 115–24. doi:10.1016/S1474-4422(06)70685-8. PMID 17239798.
^ Hart RG, Halperin JL, McBride R, Benavente O, Man-Son-Hing M, Kronmal RA (2000). "Aspirin for the primary prevention of stroke and other major vascular events: meta-analysis and hypotheses". Arch. Neurol. 57 (3): 326–32. doi:10.1001/archneur.57.3.326. PMID 10714657.
^ Bartolucci AA, Howard G (2006). "Meta-analysis of data from the six primary prevention trials of cardiovascular events using aspirin". Am. J. Cardiol. 98 (6): 746–50. doi:10.1016/j.amjcard.2006.04.012. PMID 16950176.
^ Berger JS, Roncaglioni MC, Avanzini F, Pangrazzi I, Tognoni G, Brown DL (2006). "Aspirin for the primary prevention of cardiovascular events in women and men: a sex-specific meta-analysis of randomized controlled trials". JAMA 295 (3): 306–13. doi:10.1001/jama.295.3.306. PMID 16418466.
^ Yerman T, Gan WQ, Sin DD (2007). "The influence of gender on the effects of aspirin in preventing myocardial infarction". BMC Med 5: 29. doi:10.1186/1741-7015-5-29. PMID 17949479.
^ Rothwell PM, Eliasziw M, Gutnikov SA, et al. (2003). "Analysis of pooled data from the randomised controlled trials of endarterectomy for symptomatic carotid stenosis". Lancet 361 (9352): 107–16. doi:10.1016/S0140-6736(03)12228-3. PMID 12531577.
^ Ringleb PA, Chatellier G, Hacke W, et al. (2008). "Safety of endovascular treatment of carotid artery stenosis compared with surgical treatment: a meta-analysis". J. Vasc. Surg. 47 (2): 350–5. doi:10.1016/j.jvs.2007.10.035. PMID 18241759.
^ Ederle J, Featherstone RL, Brown MM (2007). "Percutaneous transluminal angioplasty and stenting for carotid artery stenosis". Cochrane Database Syst Rev (4): CD000515. doi:10.1002/14651858.CD000515.pub3. PMID 17943745.
^ Rothwell PM, Eliasziw M, Gutnikov SA, Warlow CP, Barnett HJ (2004). "Endarterectomy for symptomatic carotid stenosis in relation to clinical subgroups and timing of surgery". Lancet 363 (9413): 915–24. doi:10.1016/S0140-6736(04)15785-1. PMID 15043958.
^ Fairhead JF, Mehta Z, Rothwell PM (2005). "Population-based study of delays in carotid imaging and surgery and the risk of recurrent stroke". Neurology 65 (3): 371–5. doi:10.1212/01.wnl.0000170368.82460.b4. PMID 16087900.
^ U.S. Preventive Services Task Force (2007). "Screening for carotid artery stenosis: U.S. Preventive Services Task Force recommendation statement". Ann. Intern. Med. 147 (12): 854–9. PMID 18087056.
^ Halliday A, Mansfield A, Marro J, et al. (2004). "Prevention of disabling and fatal strokes by successful carotid endarterectomy in patients without recent neurological symptoms: randomised controlled trial". Lancet 363 (9420): 1491–502. doi:10.1016/S0140-6736(04)16146-1. PMID 15135594.
^ Chambers BR, Donnan GA (2005). "Carotid endarterectomy for asymptomatic carotid stenosis". Cochrane Database Syst Rev (4): CD001923. doi:10.1002/14651858.CD001923.pub2. PMID 16235289.
^ Spence JD; Lees, K.; Spence, J. D. (September 2006). "Nutrition and stroke prevention". Stroke 37 (9): 2430–5. doi:10.1161/01.STR.0000236633.40160.ee. PMID 16873712.
^ Wang X, Qin X, Demirtas H, et al. (2007). "Efficacy of folic acid supplementation in stroke prevention: a meta-analysis". Lancet 369 (9576): 1876–82. doi:10.1016/S0140-6736(07)60854-X. PMID 17544768.
^ Lonn E, Yusuf S, Arnold MJ, et al. (2006). "Homocysteine lowering with folic acid and B vitamins in vascular disease". N. Engl. J. Med. 354 (15): 1567–77. doi:10.1056/NEJMoa060900. PMID 16531613.
^ Toole JF, Malinow MR, Chambless LE, et al. (2004). "Lowering homocysteine in patients with ischemic stroke to prevent recurrent stroke, myocardial infarction, and death: the Vitamin Intervention for Stroke Prevention (VISP) randomized controlled trial". JAMA 291 (5): 565–75. doi:10.1001/jama.291.5.565. PMID 14762035.
^ http://www.heartscore.org
^ Saver JL (2006). "Time is brain - quantified". Stroke 37 (37): 263–6. doi:10.1161/01.STR.0000196957.55928.ab. PMID 16339467.
^ The National Institute Of Neurological Disorders And Stroke Rt-Pa Stroke Study Group, (1995). "Tissue plasminogen activator for acute ischemic stroke. The National Institute of Neurological Disorders and Stroke rt-PA Stroke Study Group". New England Journal of Medicine 333 (24): 1581–7. doi:10.1056/NEJM199512143332401. PMID 7477192.
^ The European Cooperative Acute Stroke Study (ECASS), (2008). "Thrombolysis with Alteplase 3 to 4.5 Hours after Acute Ischemic Stroke". New England Journal of Medicine 359 (13): 1317–1329. doi:10.1056/NEJMoa0804656. PMID 18815396.
^ Dubinsky, R; Lai SM (2006). "Mortality of stroke patients treated with thrombolysis: analysis of nationwide inpatient sample". Neurology 66 (11): 1742–1744. doi:10.1212/01.wnl.0000218306.35681.38. PMID 16769953.
^ "Position Statement on the Use of Intravenous Thrombolytic Therapy in the Treatment of Stroke". American Academy of Emergency Medicine. Retrieved 2008-01-25.
^ Lee M, Hong KS, Saver JL (May 2010). "Efficacy of intra-arterial fibrinolysis for acute ischemic stroke: meta-analysis of randomized controlled trials". Stroke 41 (5): 932–7. doi:10.1161/STROKEAHA.109.574335. PMID 20360549.
^ Flint AC, Duckwiler GR, Budzik RF, Liebeskind DS, Smith WS (2007). "Mechanical thrombectomy of intracranial internal carotid occlusion: pooled results of the MERCI and Multi MERCI Part I trials". Stroke 38 (4): 1274–80. doi:10.1161/01.STR.0000260187.33864.a7. PMID 17332445.
^ Smith WS, Sung G, Starkman S, et al. (2005). "Safety and efficacy of mechanical embolectomy in acute ischemic stroke: results of the MERCI trial". Stroke 36 (7): 1432–8. doi:10.1161/01.STR.0000171066.25248.1d. PMID 15961709.
^ Lutsep HL, Rymer MM, Nesbit GM (2008). "Vertebrobasilar revascularization rates and outcomes in the MERCI and multi-MERCI trials". J Stroke Cerebrovasc Dis 17 (2): 55–7. doi:10.1016/j.jstrokecerebrovasdis.2007.11.003. PMID 18346645.
^ Smith WS (June 1, 2006). "Safety of mechanical thrombectomy and intravenous tissue plasminogen activator in acute ischemic stroke. Results of the multi Mechanical Embolus Removal in Cerebral Ischemia (MERCI) trial, part I". AJNR Am J Neuroradiol 27 (6): 1177–82. PMID 16775259.
^ Smith WS, Sung G, Saver J, et al. (2008). "Mechanical thrombectomy for acute ischemic stroke: final results of the Multi MERCI trial". Stroke 39 (4): 1205–12. doi:10.1161/STROKEAHA.107.497115. PMID 18309168.
^ Derdeyn CP, Chimowitz MI (August 2007). "Angioplasty and stenting for atherosclerotic intracranial stenosis: rationale for a randomized clinical trial". Neuroimaging Clin. N. Am. 17 (3): 355–63, viii–ix. doi:10.1016/j.nic.2007.05.001. PMID 17826637.
^ Krieger DW, De Georgia MA, Abou-Chebl A, et al. (August 2001). "Cooling for acute ischemic brain damage (cool aid): an open pilot study of induced hypothermia in acute ischemic stroke". Stroke 32 (8): 1847–54. PMID 11486115.
^ Schwab S, Schwarz S, Spranger M, Keller E, Bertram M, Hacke W (December 1998). "Moderate hypothermia in the treatment of patients with severe middle cerebral artery infarction". Stroke 29 (12): 2461–6. PMID 9836751.
^ Hart RG, Pearce LA, Aguilar MI (2007). "Meta-analysis: antithrombotic therapy to prevent stroke in patients who have nonvalvular atrial fibrillation". Ann. Intern. Med. 146 (12): 857–67. PMID 17577005.
^ Paciaroni M, Agnelli G, Micheli S, Caso V (2007). "Efficacy and safety of anticoagulant treatment in acute cardioembolic stroke: a meta-analysis of randomized controlled trials". Stroke 38 (2): 423–30. doi:10.1161/01.STR.0000254600.92975.1f. PMID 17204681. ACP JC synopsis
^ a b Coffey C. Edward, Cummings Jeffrey L, Starkstein Sergio, Robinson Robert (2000). Stroke - the American Psychiatric Press Textbook of Geriatric Neuropsychiatry (Second ed.). Washington DC: American Psychiatric Press. pp. 601–617.
^ Stanford Hospital & Clinics. "Cardiovascular Diseases: Effects of Stroke". Retrieved 2005.
^ a b Senelick Richard C., Rossi, Peter W., Dougherty, Karla (1994). Living with Stroke: A Guide for Families. Contemporary Books, Chicago. ISBN 0809226073. OCLC 42835161 40856888 42835161.
^ a b Villarosa, Linda, Ed., Singleton, LaFayette, MD, Johnson, Kirk A. (1993). Black Health Library Guide to Stroke. Henry Holt and Company, New York.
^ Reith J, Jørgensen HS, Nakayama H, Raaschou HO, Olsen TS (August 1997). "Seizures in acute stroke: predictors and prognostic significance. The Copenhagen Stroke Study". Stroke 28 (8): 1585–9. PMID 9259753.
^ Burn J, Dennis M, Bamford J, Sandercock P, Wade D, Warlow C (December 1997). "Epileptic seizures after a first stroke: the Oxfordshire Community Stroke Project". BMJ 315 (7122): 1582–7. PMID 9437276. PMC 2127973.
^ Murray CJ, Lopez AD (1997). "Mortality by cause for eight regions of the world: Global Burden of Disease Study". Lancet 349 (9061): 1269–76. doi:10.1016/S0140-6736(96)07493-4. PMID 9142060.
^ (PDF) The World health report 2004. Annex Table 2: Deaths by cause, sex and mortality stratum in WHO regions, estimates for 2002.. Geneva: World Health Organization. 2004.
^ Ellekjær, H; Holmen J, Indredavik B, Terent A (November 1, 1997). "Epidemiology of Stroke in Innherred, Norway, 1994 to 1996 : Incidence and 30-Day Case-Fatality Rate". Stroke 28 (11): 2180–2184. PMID 9368561. Retrieved 2008-01-22.
^ Bongers T, de Maat M, van Goor M et al. (2006). "High von Willebrand factor levels increase the risk of first ischemic stroke: influence of ADAMTS13, inflammation, and genetic variability". Stroke 37 (11): 2672–7. doi:10.1161/01.STR.0000244767.39962.f7. PMID 16990571.
^ Ashrafian H (2010). "Familial stroke 2700 years ago". Stroke 41 (4): e187. PMID 20185778.
^ a b Thompson JE (August 1, 1996). "The evolution of surgery for the treatment and prevention of stroke. The Willis Lecture". Stroke 27 (8): 1427–34. PMID 8711815.
^ Kopito, Jeff (September 2001). "A Stroke in Time" ([dead link]). MERGINET.com 6 (9).
^ R. Barnhart, ed. The Barnhart Concise Dictionary of Etymology (1995)
^ Schiller F (April 1970). "Concepts of stroke before and after Virchow". Med Hist 14 (2): 115–31. PMID 4914683.
[edit]Further reading
J. P. Mohr, Dennis Choi, James Grotta, Philip Wolf (2004). Stroke: Pathophysiology, Diagnosis, and Management. New York: Churchill Livingstone. ISBN 0-443-06600-0. OCLC 52990861 50477349 52990861.
Charles P. Warlow, Jan van Gijn, Martin S. Dennis, Joanna M. Wardlaw, John M. Bamford, Graeme J. Hankey, Peter A. G. Sandercock, Gabriel Rinkel, Peter Langhorne, Cathie Sudlow, Peter Rothwell (2008). Stroke: Practical Management (3rd ed.). Wiley-Blackwell. ISBN 1-4051-2766-X.
[hide]
v • d • e
CNS disease, Vascular disease: Cerebrovascular diseases (G45-G46 and I60-I69, 430-438)
Brain ischemia/
cerebral infarction
(ischemic stroke/TIA)
TACI, PACI
precerebral: Carotid artery stenosis
cerebral: MCA · ACA · Amaurosis fugax
Moyamoya disease
POCI
precerebral: Anterior spinal artery syndrome · Vertebrobasilar insufficiency (Subclavian steal syndrome)
brainstem: medulla (Medial medullary syndrome, Lateral medullary syndrome) · pons (Medial pontine syndrome/Foville's, Lateral pontine syndrome/Millard-Gubler) · midbrain (Weber's, Benedikt, Claude's)
cerebral: PCA · Lacunar stroke · Thalamic syndrome
cerebellar
General
cerebral: Cerebral venous sinus thrombosis · CADASIL · Binswanger's disease · Transient global amnesia
Intracranial hemorrhage
(hemorrhagic stroke)
Extra-axial
Epidural · Subdural · Subarachnoid
Cerebral/Intra-axial
Intraventricular
Brainstem
Duret haemorrhage
Aneurysm
Cerebral aneurysm (Intracranial berry aneurysm, Charcot-Bouchard aneurysm)
Other/general
Cerebral vasculitis
M: CNS
anat(s,m,p,4,e,b,d,c,a,f,l,g)/phys/devp/cell
noco(m,d,e,h,v,s)/cong/tumr,sysi/epon,injr
proc,drug(N1A/2AB/C/3/4/7A/B/C/D)
M: VAS
anat(a:h,u,t,a,l,v:h,u,t,a,l)/phys/devp
noco/syva/cong/tumr, sysi/epon
proc, drug(C3,C4,C5,C9)
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